Cardiac Energy Metabolism in Heart Failure

Circulation Research, Journal Year: 2021, Volume and Issue: 128(10), P. 1487 - 1513

Published: May 13, 2021

Alterations in cardiac energy metabolism contribute to the severity of heart failure. However, metabolic changes that occur failure are complex and dependent not only on type present but also co-existence common comorbidities such as obesity 2 diabetes. The failing faces an deficit, primarily because a decrease mitochondrial oxidative capacity. This is partly compensated for by increase ATP production from glycolysis. relative contribution different fuels changes, including glucose amino acid oxidation, ketone oxidation. oxidation fatty acids increases or decreases, depending For instance, associated with diabetes obesity, myocardial increases, while hypertension ischemia, decreases. Combined, these result becoming less efficient (ie, work/O consumed). alterations both glycolysis due transcriptional key enzymes involved pathways, well NAD redox state (NAD + nicotinamide adenine dinucleotide levels) metabolite signaling posttranslational epigenetic control expression genes encoding enzymes. fate glucose, beyond flux through pathology Of importance, pharmacological targeting pathways has emerged novel therapeutic approach improving efficiency, decreasing deficit function heart.

Language: Английский

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Cardiac Rehabilitation for Patients With Heart Failure

Journal of the American College of Cardiology, Journal Year: 2021, Volume and Issue: 77(11), P. 1454 - 1469

Published: March 1, 2021

Language: Английский

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Metabolic inflammation in heart failure with preserved ejection fraction

Cardiovascular Research, Journal Year: 2020, Volume and Issue: 117(2), P. 423 - 434

Published: July 7, 2020

Abstract One in 10 persons the world aged 40 years and older will develop syndrome of HFpEF (heart failure with preserved ejection fraction), most common form chronic cardiovascular disease for which no effective therapies are currently available. Metabolic disturbance inflammatory burden contribute importantly to pathogenesis. The interplay within these two biological processes is complex; indeed, it now becoming clear that notion metabolic inflammation—metainflammation—must be considered central pathophysiology. Inflammation metabolism interact over course progression, likely impact treatment prevention. Here, we discuss evidence support a causal, mechanistic role metainflammation shaping HFpEF, proposing framework comorbidities profoundly cardiac pathways syndrome.

Language: Английский

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Heart Failure with Preserved Ejection Fraction: Mechanisms and Treatment Strategies

Annual Review of Medicine, Journal Year: 2021, Volume and Issue: 73(1), P. 321 - 337

Published: Aug. 11, 2021

Approximately half of all patients with heart failure (HF) have a preserved ejection fraction, and the prevalence is growing rapidly given aging population in many countries rising obesity, diabetes, hypertension. Functional capacity quality life are severely impaired fraction (HFpEF), morbidity mortality high. In striking contrast to HF reduced there few effective treatments currently identified for HFpEF, these limited decongestion by diuretics, promotion healthy active lifestyle, management comorbidities. Improved phenotyping subgroups within overall HFpEF might enhance individualization treatment. This review focuses on current understanding pathophysiologic mechanisms underlying treatment strategies this complex syndrome.

Language: Английский

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Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: March 1, 2024

Abstract Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family (PGC-1s), consisting of three members encompassing PGC-1α, PGC-1β, and PGC-1-related coactivator (PRC), was discovered more than a quarter-century ago. PGC-1s are essential coordinators many vital cellular events, including mitochondrial functions, oxidative stress, endoplasmic reticulum homeostasis, inflammation. Accumulating evidence has shown that implicated in diseases, such as cancers, cardiac diseases cardiovascular neurological disorders, kidney motor system metabolic disorders. Examining the upstream modulators co-activated partners identifying critical biological events modulated by downstream effectors contribute to presentation elaborate network PGC-1s. Furthermore, discussing correlation between well summarizing therapy targeting helps make individualized precise intervention methods. In this review, we summarize basic knowledge regarding molecular regulatory network, discuss physio-pathological roles human review application PGC-1s, diagnostic prognostic value several therapies pre-clinical studies, suggest directions for future investigations. This presents immense potential treatment hopefully facilitates promotion new therapeutic targets.

Language: Английский

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Cardiac lipid metabolism, mitochondrial function, and heart failure

Cardiovascular Research, Journal Year: 2023, Volume and Issue: 119(10), P. 1905 - 1914

Published: June 30, 2023

A fine balance between uptake, storage, and the use of high energy fuels, like lipids, is crucial in homeostasis different metabolic tissues. Nowhere this more important precarious than heart. This highly energy-demanding muscle normally oxidizes almost all available substrates to generate energy, with fatty acids being preferred source under physiological conditions. In patients cardiomyopathies heart failure, changes main energetic substrate are observed; these hearts often prefer utilize glucose rather oxidizing acids. An imbalance uptake oxidation acid can result cellular lipid accumulation cytotoxicity. review, we will focus on sources pathways used direct cardiomyocytes. We then discuss intracellular machinery either store or oxidize lipids explain how disruptions lead mitochondrial dysfunction failure. Moreover, also role cholesterol Our discussion attempt weave vitro experiments vivo data from mice humans several human diseases illustrate metabolism gone haywire as a cause accomplice cardiac dysfunction.

Language: Английский

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Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(5), P. 2667 - 2667

Published: Feb. 25, 2024

Mitochondrial dysfunction, a feature of heart failure, leads to progressive decline in bioenergetic reserve capacity, consisting shift energy production from mitochondrial fatty acid oxidation glycolytic pathways. This adaptive process cardiomyocytes does not represent an effective strategy increase the supply and restore homeostasis thus contributing vicious circle disease progression. The increased oxidative stress causes cardiomyocyte apoptosis, dysregulation calcium homeostasis, damage proteins lipids, leakage DNA, inflammatory responses, finally stimulating different signaling pathways which lead cardiac remodeling failure. Furthermore, parallel neurohormonal with angiotensin II, endothelin-1, sympatho-adrenergic overactivation, occurs stimulates ventricular hypertrophy aggravates cellular damage. In this review, we will discuss pathophysiological mechanisms related are mainly dependent on perturbation dynamics membrane potential associated failure development We also provide overview implication mitochondria as attractive therapeutic target management recovery

Language: Английский

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Targeting HDAC6 to treat heart failure with preserved ejection fraction in mice

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: Feb. 26, 2024

Heart failure with preserved ejection fraction (HFpEF) poses therapeutic challenges due to the limited treatment options. Building upon our previous research that demonstrates efficacy of histone deacetylase 6 (HDAC6) inhibition in a genetic cardiomyopathy model, we investigate HDAC6's role HFpEF their shared mechanisms inflammation and metabolism. Here, show inhibiting HDAC6 TYA-018 effectively reverses established heart its associated symptoms male mouse models. Additionally, mice lacking Hdac6 gene, progression is delayed they are resistant TYA-018's effects. The comparable sodium-glucose cotransporter 2 (SGLT2) inhibitor, combination shows enhanced Mechanistically, restores gene expression related hypertrophy, fibrosis, mitochondrial energy production tissues. Furthermore, also inhibits activation human cardiac fibroblasts enhances respiratory capacity cardiomyocytes. In this work, findings impacts on pathophysiology promising target for treatment.

Language: Английский

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6PPD induced cardiac dysfunction in zebrafish associated with mitochondrial damage and inhibition of autophagy processes

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134357 - 134357

Published: April 21, 2024

Language: Английский

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Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease.

Kidney International, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

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