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Energy metabolism and inflammation

Energy metabolism and inflammation

Energy metabolism and inflammation in Energy metabolism and inflammation increased the intracellular level of metaoblism, thereby inhibiting Boost mental resilience accumulation of phosphofructokinase and inflammatoin, which hindered the normal progress of glycolysis Inflammation regulates fuel mobilization. The temporal risk of heart failure associated with adjuvant trastuzumab in breast cancer patients: a population study. Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide.

Energy metabolism and inflammation -

Impaired branched chain amino acid oxidation contributes to cardiac insulin resistance in heart failure.

Cardiovasc Diabetol. Sun H, Olson KC, Gao C, Prosdocimo DA, Zhou M, Wang Z, et al. Catabolic defect of branched-chain amino acids promotes heart failure. Chen M, Gao C, Yu J, Ren S, Wang M, Wynn RM, et al.

Therapeutic effect of targeting branched-chain amino acid catabolic flux in pressure-overload induced heart failure. J Am Heart Asso. Aksentijević D, Karlstaedt A, Basalay MV, O'Brien BA, Sanchez-Tatay D, Eminaga S, et al.

Intracellular sodium elevation reprograms cardiac metabolism. Nat Commun. Mullens W, Verbrugge FH, Nijst P, Tang WHW. Renal sodium avidity in heart failure: from pathophysiology to treatment strategies.

Eur Heart J. Baartscheer A, Schumacher CA, van Borren MM, Belterman CN, Coronel R, Fiolet JW. Cardiovasc Res. Eisner DA, Caldwell JL, Trafford AW, Hutchings DC. The control of diastolic calcium in the heart: basic mechanisms and functional implications.

Boyman L, Karbowski M, Lederer WJ. Trends Mol Med. Dridi H, Kushnir A, Zalk R, Yuan Q, Melville Z, Marks AR. Intracellular calcium leak in heart failure and atrial fibrillation: a unifying mechanism and therapeutic target. Ruiz-Meana M, Minguet M, Bou-Teen D, Miro-Casas E, Castans C, Castellano J, et al.

Ryanodine receptor glycation favors mitochondrial damage in the senescent heart. Calcium signaling and reactive oxygen species in mitochondria. Zhang J, Abel ED. Effective metabolic approaches for the energy starved failing heart: bioenergetic resiliency via redundancy or something else?

Ardehali H, Sabbah HN, Burke MA, Sarma S, Liu PP, Cleland JG, et al. Targeting myocardial substrate metabolism in heart failure: potential for new therapies. Eur J Heart Fail. Chen Z, Liu M, Li L, Chen L. Involvement of the Warburg effect in non-tumor diseases processes.

J Cell Physiol. Briasoulis A, Androulakis E, Christophides T, Tousoulis D. The role of inflammation and cell death in the pathogenesis, progression and treatment of heart failure. Heart Fail Rev. Chow SL, Maisel AS, Anand I, Bozkurt B, de Boer RA, Felker GM, et al.

Role of biomarkers for the prevention, assessment, and management of heart failure: a scientific statement from the American heart association. Emdin M, Aimo A, Vergaro G, Bayes-Genis A, Lupón J, Latini R, et al.

sST2 predicts outcome in chronic heart failure beyond NT-proBNP and high-sensitivity troponin T. J Am Coll Cardiol. Martini E, Kunderfranco P, Peano C, Carullo P, Cremonesi M, Schorn T, et al. Single-cell sequencing of mouse heart immune infiltrate in pressure overload-driven heart failure reveals extent of immune activation.

Abplanalp WT, Cremer S, John D, Hoffmann J, Schuhmacher B, Merten M, et al. Clonal hematopoiesis-driver DNMT3A mutations alter immune cells in heart failure. Adamo L, Rocha-Resende C, Prabhu SD, Mann DL. Reappraising the role of inflammation in heart failure.

Frangogiannis NG. Regulation of the inflammatory response in cardiac repair. Chen D, Assad-Kottner C, Orrego C, Torre-Amione G.

Cytokines and acute heart failure. Crit Care Med. Lin HB, Naito K, Oh Y, Farber G, Kanaan G, Valaperti A, et al. McMaster WG, Kirabo A, Madhur MS, Harrison DG. Inflammation, immunity, and hypertensive end-organ damage.

Sanada S, Hakuno D, Higgins LJ, Schreiter ER, McKenzie AN, Lee RT. IL and ST2 comprise a critical biomechanically induced and cardioprotective signaling system.

Paulus WJ. Unfolding discoveries in heart failure. Toldo S, Abbate A. The NLRP3 inflammasome in acute myocardial infarction.

The extracellular matrix in ischemic and nonischemic heart failure. Brakenhielm E, González A, Díez J. Role of cardiac lymphatics in myocardial edema and fibrosis: JACC review topic of the week.

Westermann D, Kasner M, Steendijk P, Spillmann F, Riad A, Weitmann K, et al. Role of left ventricular stiffness in heart failure with normal ejection fraction. Ling LH, Kistler PM, Kalman JM, Schilling RJ, Hunter RJ.

Comorbidity of atrial fibrillation and heart failure. van den Berg MP, Mulder BA, Klaassen SHC, Maass AH, van Veldhuisen DJ, van der Meer P, et al. Heart failure with preserved ejection fraction, atrial fibrillation, and the role of senile amyloidosis.

Santhanakrishnan R, Wang N, Larson MG, Magnani JW, McManus DD, Lubitz SA, et al. Atrial fibrillation begets heart failure and vice versa: temporal associations and differences in preserved versus reduced ejection fraction.

Wong JA, Conen D, Van Gelder IC, McIntyre WF, Crijns HJ, Wang J, et al. Progression of device-detected subclinical atrial fibrillation and the risk of heart failure. Patel RB, Vaduganathan M, Shah SJ, Butler J. Atrial fibrillation in heart failure with preserved ejection fraction: insights into mechanisms and therapeutics.

Yoo S, Aistrup G, Shiferaw Y, Ng J, Mohler PJ, Hund TJ, et al. Oxidative stress creates a unique, CaMKII-mediated substrate for atrial fibrillation in heart failure. JCI Insight. Kutyifa V, Vermilye K, Solomon SD, McNitt S, Moss AJ, Daimee UA. Long-term outcomes of cardiac resynchronization therapy by left ventricular ejection fraction.

Wijesurendra RS, Casadei B. Mechanisms of atrial fibrillation. Ballou LM, Lin RZ, Cohen IS. Control of cardiac repolarization by phosphoinositide 3-kinase signaling to ion channels. Seferović PM, Petrie MC, Filippatos GS, Anker SD, Rosano G, Bauersachs J, et al.

Type 2 diabetes mellitus and heart failure: a position statement from the heart failure association of the European society of cardiology. Euro J Heart Fail.

Greene SJ, Vaduganathan M, Khan MS, Bakris GL, Weir MR, Seltzer JH, et al. Prevalent and incident heart failure in cardiovascular outcome trials of patients with type 2 diabetes. Rørth R, Jhund PS, Mogensen UM, Kristensen SL, Petrie MC, Køber L, et al.

Risk of incident heart failure in patients with diabetes and asymptomatic left ventricular systolic dysfunction.

Diab Care. Rawshani A, Rawshani A, Sattar N, Franzén S, McGuire DK, Eliasson B, et al. Relative prognostic importance and optimal levels of risk factors for mortality and cardiovascular outcomes in type 1 diabetes mellitus.

Dillmann WH. Diabetic cardiomyopathy. Taqueti VR, Di Carli MF. Coronary microvascular disease pathogenic mechanisms and therapeutic options: JACC state-of-the-art review. Riehle C, Abel ED.

Insulin signaling and heart failure. Donath MY, Meier DT, Boni-Schnetzler M. Inflammation in the pathophysiology and therapy of cardiometabolic disease.

Endocr Rev. Fernandez-Ruiz I. A new link for heart failure and diabetes. Papadaki M, Holewinski RJ, Previs SB, Martin TG, Stachowski MJ, Li A, et al. Diabetes with heart failure increases methylglyoxal modifications in the sarcomere, which inhibit function.

Kenny HC, Abel ED. Heart failure in type 2 diabetes mellitus. Packer M. Activation and inhibition of sodium-hydrogen exchanger is a mechanism that links the pathophysiology and treatment of diabetes mellitus with that of heart failure.

Shah MS, Brownlee M. Molecular and cellular mechanisms of cardiovascular disorders in diabetes. Rutten FH, Cramer MJ, Lammers JW, Grobbee DE, Hoes AW. Heart failure and chronic obstructive pulmonary disease: an ignored combination? Carter P, Lagan J, Fortune C, Bhatt DL, Vestbo J, Niven R, et al.

Association of cardiovascular disease with respiratory disease. Ramalho SHR, Shah AM. Lung function and cardiovascular disease: a link. Trends Cardiov Med. Canepa M, Straburzynska-Migaj E, Drozdz J, Fernandez-Vivancos C, Pinilla JMG, Nyolczas N, et al.

Characteristics, treatments and 1-year prognosis of hospitalized and ambulatory heart failure patients with chronic obstructive pulmonary disease in the European society of cardiology heart failure long-term registry.

Morgan AD, Rothnie KJ, Bhaskaran K, Smeeth L, Quint JK. Chronic obstructive pulmonary disease and the risk of 12 cardiovascular diseases: a population-based study using UK primary care data. Roversi S, Fabbri LM, Sin DD, Hawkins NM, Agustí A. Chronic obstructive pulmonary disease and cardiac diseases.

An urgent need for integrated care. Am J Respir Crit Care Med. Singh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli BR, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease: the GOLD science committee report Eur Respir J.

Stone IS, Barnes NC, James WY, Midwinter D, Boubertakh R, Follows R. Lung deflation and cardiovascular structure and function in chronic obstructive pulmonary disease. A randomized controlled trial.

Hawkins NM, Virani S, Ceconi C. Heart failure and chronic obstructive pulmonary disease: the challenges facing physicians and health services.

Rocha A, Arbex FF, Sperandio PA, Souza A, Biazzim L, Mancuso F, et al. Excess ventilation in chronic obstructive pulmonary disease-heart failure overlap. Implications for dyspnea and exercise intolerance. Horwich TB, Broderick S, Chen L, McCullough PA, Strzelczyk T, Kitzman DW, et al.

Relation among body mass index, exercise training, and outcomes in chronic systolic heart failure. Am J Cardiol. Kapoor JR, Heidenreich PA. Obesity and survival in patients with heart failure and preserved systolic function: a U-shaped relationship.

Am Heart J. Pandey A, LaMonte M, Klein L, Ayers C, Psaty BM, Eaton CB, et al. Relationship between physical activity, body mass index, and risk of heart failure. Streng KW, Voors AA, Hillege HL, Anker SD, Cleland JG, Dickstein K, et al. Waist-to-hip ratio and mortality in heart failure.

Tsujimoto T, Kajio H. Abdominal obesity is associated with an increased risk of all-cause mortality in patients with HFpEF. Obesity-associated heart failure as a theoretical target for treatment with mineralocorticoid receptor antagonists.

JAMA Cardiol. Lavie CJ, Ozemek C, Carbone S, Katzmarzyk PT, Blair SN. Sedentary behavior, exercise, and cardiovascular health. Mouton AJ, Li X, Hall ME, Hall JE. Obesity, hypertension, and cardiac dysfunction: novel roles of immunometabolism in macrophage activation and inflammation.

Sweeney G. Cardiovascular effects of leptin. Leptin-aldosterone-neprilysin axis: identification of its distinctive role in the pathogenesis of the three phenotypes of heart failure in people with obesity. Mechanick JI, Farkouh ME, Newman JD, Garvey WT. Cardiometabolic-based chronic disease, adiposity and dysglycemia drivers: JACC state-of-the-art review.

Abel ED, Litwin SE, Sweeney G. Cardiac remodeling in obesity. Suthahar N, Meijers WC, Ho JE, Gansevoort RT, Voors AA, van der Meer P, et al. Sex-specific associations of obesity and N-terminal pro-B-type natriuretic peptide levels in the general population. Nadruz W Jr, Claggett BL, McMurray JJ, Packer M, Zile MR, et al.

Impact of body mass index on the accuracy of n-terminal pro-brain natriuretic peptide and brain natriuretic peptide for predicting outcomes in patients with chronic heart failure and reduced ejection fraction: insights from the PARADIGM-HF study prospective comparison of ARNI with ACEI to determine impact on global mortality and morbidity in heart failure trial.

Kälsch H, Neumann T, Erbel R. Less increase of BNP and NT-proBNP levels in obese patient with decompensated heart failure: interpretation of natriuretic peptides in obesity.

Int J Cardiol. Díez J. Chronic heart failure as a state of reduced effectiveness of the natriuretic peptide system: implications for therapy. de Boer RA, Hulot JS, Tocchetti CG, Aboumsallem JP, Ameri P, Anker SD, et al.

Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the translational research committee of the heart failure association HFA of the European society of cardiology ESC.

de Boer RA, Meijers WC, van der Meer P, van Veldhuisen DJ. Cancer and heart disease: associations and relations. Anker MS, Sanz AP, Zamorano JL, Mehra MR, Butler J, Riess H, et al. Advanced cancer is also a heart failure syndrome - an hypothesis. Libby P, Sidlow R, Lin AE, Gupta D, Jones LW, Moslehi J, et al.

Clonal hematopoiesis: crossroads of aging, cardiovascular disease, and cancer: JACC review topic of the week. Varga ZV, Ferdinandy P, Liaudet L, Pacher P. Drug-induced mitochondrial dysfunction and cardiotoxicity.

Am J Physiol Heart Circul Physiol. Liu Y, Asnani A, Zou L, Bentley VL, Yu M, Wang Y, et al. Visnagin protects against doxorubicin-induced cardiomyopathy through modulation of mitochondrial malate dehydrogenase.

Sci Trans Med. Pudil R, Mueller C, Celutkiene J, Henriksen PA, Lenihan D, Dent S, et al. Role of serum biomarkers in cancer patients receiving cardiotoxic cancer therapies: a position statement from the cardio-oncology study group of the heart failure association and the cardio-oncology council of the european society of cardiology.

Khosrow-Khavar F, Filion KB, Bouganim N, Suissa S, Azoulay L. Aromatase inhibitors and the risk of cardiovascular outcomes in women with breast cancer: a population-based cohort study. Boekel NB, Duane FK, Jacobse JN, Hauptmann M, Schaapveld M, Sonke GS, et al.

Heart failure after treatment for breast cancer. Banke A, Fosbøl EL, Møller JE, Gislason GH, Andersen M, Bernsdorf M, et al. Long-term effect of epirubicin on incidence of heart failure in women with breast cancer: insight from a randomized clinical trial. Salz T, Zabor EC, de Nully Brown P, Dalton SO, Raghunathan NJ, Matasar MJ, et al.

Preexisting cardiovascular risk and subsequent heart failure among non-hodgkin lymphoma survivors. J Clin Oncol. Goldhar HA, Yan AT, Ko DT, Earle CC, Tomlinson GA, Trudeau ME, et al.

The temporal risk of heart failure associated with adjuvant trastuzumab in breast cancer patients: a population study. J Nation Cancer Inst. Zhang S, Liu X, Bawa-Khalfe T, Lu LS, Lyu YL, Liu LF, et al. Identification of the molecular basis of doxorubicin-induced cardiotoxicity.

Nat Med. Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM, et al. Lara KM, Levitan EB, Gutierrez OM, Shikany JM, Safford MM, Judd SE, et al. Dietary patterns and incident heart failure in U. Adults without known coronary disease. Larsson SC, Orsini N, Wolk A. Alcohol consumption and risk of heart failure: a dose-response meta-analysis of prospective studies.

Schloss MJ, Swirski FK, Nahrendorf M. Modifiable cardiovascular risk, hematopoiesis, and innate immunity. Chudasama YV, Khunti K, Gillies CL, Dhalwani NN, Davies MJ, Yates T, et al. Healthy lifestyle and life expectancy in people with multimorbidity in the UK biobank: a longitudinal cohort study.

Barnes PJ. Mechanisms of development of multimorbidity in the elderly. Forman DE, Maurer MS, Boyd C, Brindis R, Salive ME, Horne FM, et al. Multimorbidity in older adults with cardiovascular disease.

Sharma K, Kass DA. Heart failure with preserved ejection fraction. Cir Res. Ajoolabady A, Aslkhodapasandhokmabad H, Aghanejad A, Zhang Y, Ren J.

Mitophagy receptors and mediators: therapeutic targets in the management of cardiovascular ageing. Ageing Res Rev. Lesnefsky EJ, Chen Q, Hoppel CL.

Mitochondrial metabolism in aging heart. Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Miyamoto S. Autophagy and cardiac aging. Cell Death Diff. Sack MN, Fyhrquist FY, Saijonmaa OJ, Fuster V, Kovacic JC.

Basic biology of oxidative stress and the cardiovascular system: part 1 of a 3-part series. Ng R, Sutradhar R, Yao Z, Wodchis WP, Rosella LC.

Smoking, drinking, diet and physical activity-modifiable lifestyle risk factors and their associations with age to first chronic disease.

Int J Epidemiol. Harrington JL, Ayers C, Berry JD, Omland T, Pandey A, Seliger SL, et al. Sedentary behavior and subclinical cardiac injury: results from the dallas heart study. Bricca A, Harris LK, Jäger M, Smith SM, Juhl CB, Skou ST. Benefits and harms of exercise therapy in people with multimorbidity: a systematic review and meta-analysis of randomised controlled trials.

Gan Z, Fu T, Kelly DP, Vega RB. Skeletal muscle mitochondrial remodeling in exercise and diseases. Cell Res. Vega RB, Konhilas JP, Kelly DP, Leinwand LA. Molecular mechanisms underlying cardiac adaptation to exercise.

Cell Metabo. Karstoft K, Pedersen BK. Exercise and type 2 diabetes: focus on metabolism and inflammation. Immunol Cell Biol. Zhou Y, Zhou B, Pache L, Chang M, Khodabakhshi AH, Tanaseichuk O, et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets.

Han H, Cho JW, Lee S, Yun A, Kim H, Bae D, et al. TRRUST v2: an expanded reference database of human and mouse transcriptional regulatory interactions. Nucleic Acids Res. Zhang Y, Murugesan P, Huang K, Cai H. NADPH oxidases and oxidase crosstalk in cardiovascular diseases: novel therapeutic targets.

Hoes MF, Grote Beverborg N, Kijlstra JD, Kuipers J, Swinkels DW, Giepmans BNG, et al. Iron deficiency impairs contractility of human cardiomyocytes through decreased mitochondrial function. Maillet M, van Berlo JH, Molkentin JD. Molecular basis of physiological heart growth: fundamental concepts and new players.

Nat Rev Mol Cell Biol. Zhao Z, Li R, Wang X, Li J, Yuan M, Liu E, et al. Cardiovasc Drugs Ther. Barnes PJ, Baker J, Donnelly LE. Cellular senescence as a mechanism and target in chronic lung diseases. An R, Zhao L, Xi C, Li H, Shen G, Liu H, et al.

Belaidi E, Morand J, Gras E, Pépin JL, Godin-Ribuot D. Targeting the ROS-HIFendothelin axis as a therapeutic approach for the treatment of obstructive sleep apnea-related cardiovascular complications.

Khan MI, Rath S, Adhami VM, Mukhtar H. Hypoxia driven glycation: mechanisms and therapeutic opportunities. Sem Cancer Biol. Sundaresan NR, Vasudevan P, Zhong L, Kim G, Samant S, Parekh V, et al. The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun.

Wo D, Peng J, Ren DN, Qiu L, Chen J, Zhu Y, et al. Luczak ED, Wu Y, Granger JM, Joiner MA, Wilson NR, Gupta A, et al. Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.

Pfleger J, Gresham K, Koch WJ. G protein-coupled receptor kinases as therapeutic targets in the heart. Sidlow R, Lin AE, Gupta D, Bolton KL, Steensma DP, Levine RL, et al. The clinical challenge of clonal hematopoiesis, a newly recognized cardiovascular risk factor.

Meng L, Li XY, Shen L, Ji HF. Type 2 diabetes mellitus drugs for alzheimer's disease: current evidence and therapeutic opportunities. Koitabashi N, Kass DA.

Reverse remodeling in heart failure—mechanisms and therapeutic opportunities. Tousoulis D, Oikonomou E, Siasos G, Stefanadis C. Statins in heart failure—With preserved and reduced ejection fraction.

An update. Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy. Venot Q, Blanc T, Rabia SH, Berteloot L, Ladraa S, Duong JP, et al. Targeted therapy in patients with PIK3CA-related overgrowth syndrome.

Faria A, Persaud SJ. Cardiac oxidative stress in diabetes: mechanisms and therapeutic potential. Chan JY, Chan SH. Activation of endogenous antioxidants as a common therapeutic strategy against cancer, neurodegeneration and cardiovascular diseases: a lesson learnt from DJ Brown DA, Perry JB, Allen ME, Sabbah HN, Stauffer BL, Shaikh SR, et al.

Expert consensus document: mitochondrial function as a therapeutic target in heart failure. Lam CSP, Voors AA, de Boer RA, Solomon SD, van Veldhuisen DJ. Heart failure with preserved ejection fraction: from mechanisms to therapies. Rocha M, Apostolova N, Diaz-Rua R, Muntane J, Victor VM.

Mitochondria and T2D: role of autophagy, ER stress, and inflammasome. Trends Endocrinol Metab. Koliaki C, Roden M. Alterations of mitochondrial function and insulin sensitivity in human obesity and diabetes mellitus. Ann Rev Nutr. Rowlands DJ. Mitochondria dysfunction: a novel therapeutic target in pathological lung remodeling or bystander?

Piantadosi CA, Suliman HB. Mitochondrial dysfunction in lung pathogenesis. Ann Rev Physiol. Morava E, Kozicz T. Mitochondria and the economy of stress mal adaptation.

Neuro Bio Rev. van der Meer P, van der Wal HH, Melenovsky V. Mitochondrial function, skeletal muscle metabolism, and iron deficiency in heart failure. Khan RS, Bril F, Cusi K, Newsome PN. Modulation of insulin resistance in nonalcoholic fatty liver disease. Mesarwi OA, Loomba R, Malhotra A.

Obstructive sleep apnea, hypoxia, and nonalcoholic fatty liver disease. Forbes JM, Thorburn DR. Mitochondrial dysfunction in diabetic kidney disease.

Nat Rev Nephrol. Autophagy-dependent and -independent modulation of oxidative and organellar stress in the diabetic heart by glucose-lowering drugs. Javadov S, Jang S, Agostini B.

Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives. Delbridge LMD, Mellor KM, Taylor DJ, Gottlieb RA.

Myocardial stress and autophagy: mechanisms and potential therapies. Neeland IJ, Poirier P, Després JP. Cardiovascular and metabolic heterogeneity of obesity: clinical challenges and implications for management.

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Kaplanski G. Interleukin biological properties and role in disease pathogenesis. Immunol Rev. Pinar AA, Scott TE, Huuskes BM, Tapia Cáceres FE, Kemp-Harper BK, Samuel CS. Targeting the NLRP3 inflammasome to treat cardiovascular fibrosis.

Birrell MA, Eltom S. The role of the NLRP3 inflammasome in the pathogenesis of airway disease. Wada J, Makino H. Innate immunity in diabetes and diabetic nephropathy. Komada T, Muruve DA. The role of inflammasomes in kidney disease.

Livshits G, Kalinkovich A. Inflammaging as a common ground for the development and maintenance of sarcopenia, obesity, cardiomyopathy and dysbiosis. McElvaney OJ, McEvoy NL, McElvaney OF, Carroll TP, Murphy MP, Dunlea DM.

Characterization of the inflammatory response to severe COVID illness. Sanders-van Wijk S, Tromp J, Beussink-Nelson L, Hage C, Svedlund S, Saraste A, et al. Proteomic evaluation of the comorbidity-inflammation paradigm in heart failure with preserved ejection fraction: results from the PROMIS-HFpEF study.

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Mortality associated with heart failure with preserved vs. Reduced ejection fraction in a prospective international multi-ethnic cohort study. Physical activities consume a major portion of energy in our daily life, which are usually reduced in the aging population.

This reduction in energy expenditure may lead to energy accumulation in the body and consequently a gain in adiposity. In obesity, systemic chronic inflammation occurs with elevated proinflammatory cytokines IL-6, MCP-1, CRP, PAI-1, et al. in the circulation.

The systemic inflammation is due to an inflammatory response in adipose tissues that are under quick expansion. Adipocytes produce these cytokines. In addition, macrophage infiltration into the adipose tissue contributes significantly to the cytokine production.

Although we have learned a lot about the signaling pathways that link energy accumulation adiposity to chronic inflammation, we know little about the real biological significance of the inflammation.

This article addresses this issue, and provides an overview of the interaction of inflammation and energy balance. In obesity research, the link between chronic inflammation and energy fat accumulation is well established.

The initial observation of TNF-α elevation in adipose tissue of obese mice provides the first evidence for the chronic inflammation in by Hotamisligil and colleagues [ 4 ]. Thereafter, the concept was enforced by abundant literature identifying increases in many other inflammatory cytokines, such as plasma C-reactive protein CRP , interleukin 6 IL-6 , plasminogen activator inhibitor-1 PAI-1 , in models of obesity.

Activation of inflammatory kinases such as IKKβ IkBα kinase beta and JNK1 c-Jun N-terminal kinase 1 provides additional evidence for activation of intracellular inflammatory pathways in obesity [ 5 - 6 ]. Obesity-associated inflammation is chronic, systemic, low-grade, and not linked to any infection.

In contrast to inflammation induced by bacteria or virus infection where neutrophil granulocytes are elevated in the circulation, neutrophil granulocytes are not increased in blood in obesity. The inflammation is systemic since the inflammatory cytokines are increased in the circulation. The metabolites of fatty acids and glucose include diaglyceride DAG , Ceramide, and reactive oxygen species Figure 1.

They activate inflammatory response through several approaches. They may direct interact with signaling kinases PKCs, JNKs and IKKs in cells [ 7 ]. They may also act through cell membrane receptors for lipids, such as TLR4, CD36 or GPR [ 8 - 11 ].

The reactive oxygen species ROS are generated from fat or glucose oxidation in mitochondria. ROS may induce activation of the inflammatory kinases JNK and IKK. The lipids also induce endoplasmic reticulum ER stress for activation of JNK and IKK [ 12 - 13 ].

In CR, these metabolites of glucose and fatty acids are reduced from less calorie intake. The risk of inflammation is reduced.

In obesity, adipose tissue is a major source of chronic inflammation [ 14 - 15 ]. In adipose tissue, adipocytes and adipose tissue macrophages ATM are the major cell types responsible for the production of inflammatory cytokines.

The representative cytokines include TNF-α, IL-6, MCP-1 and PAI Adipokines Leptin and adiponectin are produced by adipocytes and also involved in the regulation of inflammation. Macro-phages and adipocytes are activated during the process of adipose tissue expansion.

Recent studies suggest that the adipose tissue expansion induces a local hypoxia response [ 16 ]. The hypoxia response serves as a common root for all of the stress responses in adipose tissue, such as oxidative stress, ER stress, and inflammatory stress [ 17 - 19 ].

Hypoxia directly promotes the chronic inflammation through activation of transcription factors NF-kB and HIF-1 in adipocytes and macrophages [ 16 ]. The hypoxia response is a result of tissue expansion.

In CR, adipose tissue expansion is reduced or under controlled. The risk factors for inflammation, such as adipose tissue hypoxia, lipid accumulation, ER stress and oxidative stress are all reduced or absent. These may explain why CR reduces the risk for chronic inflammation in the body.

Figure 1. Energy accumulation induces inflammation. Energy accumulation leads to elevation in glucose and fatty acids. These substrates lead to production of diaglycerids DAG , Ceramide, reactive oxygen species ROS and activation of toll-like receptor 4 TLR4 in cells including macrophages and endothelial cells.

As a consequence, expression of inflammatory cytokines and adhesion molecules may increase for chronic local inflammation. When inflammatory cytokines are elevated in the circulation, the energy accumulation causes systemic chronic inflammation, which is observed in obesity.

This kind of chronic inflammation is limited or prevented by calorie restriction. The inflammation observed in adipose tissue likely serves as a feedback signal locally in adipose tissue and systemically for energy expenditure Figure 2.

In adipose tissue, inflammation inhibits adipocyte expansion and adipocyte differentiation, changes adipocyte endocrine and induces extracellular matrix remodeling [ 20 ]. The local response is translated into a systemic response through cytokines and free acids released from adipose tissue.

Figure 2. Inflammation in obesity. Rapid growth of adipose tissue leads to quick expansion of adipose tissue. When angiogenesis or vessel dilation can not meet the demand for blood supply, there will be an adipose tissue hypoxia ATH from lack of blood supply.

ATH will induce angiogenesis and trigger inflammation. Inflammation will promote angiogenesis and vasodilation locally in the tissue for extracellular remodeling. When inflammatory cytokines and fatty acids are elevated in the circulation, they will promote energy expenditure systemically.

The inflammatory response may also induce hyperglycemia and energy disposal through glucose excretion in urine. In this way, inflammation acts through insulin resistance and hyperglycemia.

a Adipocyte inhibition. A major function of adipocytes is to store fat. Inflammatory cytokines inhibit adipocyte function in multiple aspects. These include inhibition of preadipocyte differentiation, induction of lipolysis and suppression of adiponectin expression in mature adipocytes.

These inhibitory activities are well documented for TNF-α and IL-1 [ 21 - 23 ]. At the molecular level, inflammation inhibits insulin signaling pathway [ 24 - 26 ] and PPARγ activities in adipocytes [ 27 ]. These effects contribute to suppression of tissue expansion, and alteration in cytokine profile.

The disorders in lipid metabolism and cytokine balance contribute to the whole body insulin resistance, a result of impaired insulin signaling in multiple organs skeletal muscle, liver, and adipose tissue [ 28 - 30 ].

Insulin resistance may induce hyperglycemia, which in turn leads to glucose excretion through urine type 2 diabetes. The type 2 diabetes is an extreme condition in the body to get ride of energy surplus in an effort to prevent energy accumulation in the body. b Adipose tissue remodeling: Macrophage infiltration is a major marker of local inflammation in the adipose tissue in obesity.

Adipose tissue macrophages ATM have been under active investigation since when macrophage infiltration was initially identified in obese mice [ 31 - 34 ].

The discovery provides a source for TNF-α in adipose tissue since mature adipocytes produces very little TNF-α [ 31 - 34 ]. The biological significance of macrophage infiltration remains to be elucidated. However, more and more evidence suggests that macrophages are required for adipose tissue remodeling and adipogenesis of preadipocytes.

Macrophages may serve as a signal amplifier in the adipose tissue for stimulation of angiogenesis [ 35 ]. Macrophages produce many angiogenic factors, such as PDGF, TGF-β and HGF, which are increased in adipose tissue in obese individuals [ 36 - 37 ]. Interestingly, this activity of macrophages is required for adipose tissue growth in lean mice [ 38 - 39 ] and obese mice [ 35 ].

Macrophages may also regulate blood flow through production of vasodilators such as NO. Macrophages may clean the cell debris of dead adipocytes within the adipose tissue [ 40 ].

An increase in adipocyte death was reported in the adipose tissue of obese mice, and the dead cells were surrounded by ATMs to form the "Crown" like structure [ 40 - 41 ]. The cell death in adipose tissue may be a result of the hypoxia response [ 42 ]. In CR, the adipose tissue expansion is under control, there are not such risk factors for macrophage activation in adipose tissue.

c Fuel mobilization. Inflammation regulates fuel mobilization. The role of inflammatory cytokines has drawn a lot of attention in the fuel mobilization. Cytokines such as TNF-α, IL-1, IL-6, et al. FFAs are normally oxidized in mitochondria for ATP production.

An increase in FFA supply may lead to acceleration of energy expenditure. However, when FFA supply overrides the consumption, they deposit in non-adipocytes in the form of ectopic fat deposition.

The ectopic fat contributes to pathogenesis of fatty liver disease and atherosclosis deposit on the blood vessel wall.

In the physiological conditions, IL-6 secreted by contracting muscle is involved in coordination of fuel mobilization between adipose tissue and skeletal muscle during exercise [ 43 - 44 ]. In CR, the fatty acid supply is limited as a result of reduced calorie intake, the risk for ectopic fat deposition will be reduced.

This may help in prevention of fatty liver and atherosclosis. d Energy intake. Inflammatory cytokines are involved in the regulation of energy intake and expenditure. IL-1 and IL-6 reduces food intake and prevent hyperphagia [ 45 - 46 ]. Cytokines IL-1, IL-6 and TNF-α also induce energy expenditure [ 46 - 50 ].

These activities of cytokines are dependent on their actions in the central nervous system [ 46 - 47 , 51 - 52 ]. Therefore, inflammatory cytokines may serve as an anti-obesity signal by modifying both energy intake and energy expenditure.

Additionally, these data indicate that the inflammatory cytokines may serve as a link between peripheral tissues and central nervous system in the control of energy balance.

The activities of inflammatory cytokines on adipocytes and neurons suggest that inflammation may inhibit energy accumulation. They induce energy expenditure and inhibits food intake.

These possibilities are strongly supported by phenotypes of transgenic mice with chronic inflammation and by cytokine infusion studies. The pathway has been under active investigation in the obesity field after IKKβ was found to induce insulin resistance in obese mice [ 5 ].

Ye JKeller JN. Regulation of emtabolism metabolism Energy metabolism and inflammation inflmamation A Energy metabolism and inflammation response inflammatipn obesity and calorie restriction. Aging Albany NY. Copyright: © Ye et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Protein Metabolism Overview, Animation Niflammation important metabolic substrates, Rebalance amino acids BCAAs Enerby fatty acids FAs participate in metsbolism significant physiological processes, such as mitochondrial Energy metabolism and inflammation, ihflammation metabolism, Energy metabolism and inflammation inflammation, anf with intermediate znd generated inflam,ation their catabolism. The increased levels of BCAAs and fatty acids Energy metabolism and inflammation lead to mitochondrial dysfunction inflmmation altering mitochondrial biogenesis and adenosine triphosphate ATP production metabilism interfering with glycolysis, fatty acid oxidation, the tricarboxylic acid cycle TCA cycle, and oxidative phosphorylation. BCAAs can directly activate the mammalian target of rapamycin mTOR signaling pathway to induce insulin resistance, or function together with fatty acids. In addition, elevated levels of BCAAs and fatty acids can activate the canonical nuclear factor-κB NF-κB signaling pathway and inflammasome and regulate mitochondrial dysfunction and metabolic disorders through upregulated inflammatory signals. This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically. Carbohydrates, lipids, and amino acids are the three major nutrients for humans. They are oxidized, and they supply energy in various ways to maintain activities of the body. Energy metabolism and inflammation

Author: Shakinos

1 thoughts on “Energy metabolism and inflammation

  1. Sie haben ins Schwarze getroffen. Mir scheint es der gute Gedanke. Ich bin mit Ihnen einverstanden.

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