ArticleCardiovascular research2018
Enhancing fatty acid utilization ameliorates mitochondrial fragmentation and cardiac dysfunction via rebalancing optic atrophy 1 processing in the failing heart.
Article in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 70 citations in OpenAlex.
- Loss of Rab8a-Dependent Tethering of Lipid Droplets to Mitochondria Contributes to Hypoxia-Reoxygenation Injury.MedComm · 2026Article
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- A high-fat diet nutritional intervention reprograms cardiac metabolism and improves systolic function in a pig model of heart failure with reduced ejection fraction.Basic research in cardiology · 2026Article
- Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.BMC cardiovascular disorders · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- The crosstalk between mitochondrial dysfunction and fatty acid metabolism in heart failure: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Activation of AMPK/OPA1 pathway alleviates traumatic brain damage by regulating mitophagy.Acta cirurgica brasileira · 2025Article
- Cardiac Urea Cycle Activation by Time-Restricted Feeding Protects Against Pressure Overload-Induced Heart Failure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitophagy deficiency activates stimulator of interferon genes activation and aggravates pathogenetic cardiac remodeling.Genes & diseases · 2024Article
- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- Mechanisms involved in the regulation of mitochondrial quality control by PGAM5 in heart failure.Cell stress & chaperones · 2024Review
- Succinate dehydrogenase is essential for epigenetic and metabolic homeostasis in hearts.Basic research in cardiology · 2023Article
- Flt3 Activation Mitigates Mitochondrial Fragmentation and Heart Dysfunction through Rebalanced L-OPA1 Processing by Hindering the Interaction between Acetylated p53 and PHB2 in Cardiac Remodeling.Antioxidants (Basel, Switzerland) · 2023Article
- Low-carbohydrate diets containing plant-derived fat but not animal-derived fat ameliorate heart failure.Scientific reports · 2023Article
- Comprehensive Analysis of Mitochondrial Dynamics Alterations in Heart Diseases.International journal of molecular sciences · 2023Review
- iNOS aggravates pressure overload-induced cardiac dysfunction via activation of the cytosolic-mtDNA-mediated cGAS-STING pathway.Theranostics · 2023Article
- The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.The journal of cardiovascular aging · 2023Article
- Pharmacological inhibition of adipose tissue adipose triglyceride lipase by Atglistatin prevents catecholamine-induced myocardial damage.Cardiovascular research · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Heart failure (HF) is characterized by reduced fatty acid (FA) utilization associated with mitochondrial dysfunction. Recent evidence has shown that enhancing FA utilization may provide cardioprotection against HF. Our aim was to investigate the effects and the underlying mechanisms of cardiac FA utilization on cardiac function in response to pressure overload. Methods and results: Transverse aortic constriction (TAC) was used in C57 mice to establish pressure overload-induced HF. TAC mice fed on a high fat diet (HFD) exhibited increased cardiac FA utilization and improved cardiac function and survival compared with those on control diet. Such cardioprotection could also be provided by cardiac-specific overexpression of CD36. Notably, both HFD and CD36 overexpression attenuated mitochondrial fragmentation and improved mitochondrial function in the failing heart. Pressure overload decreased ATP-dependent metalloprotease (YME1L) expression and induced the proteolytic cleavage of the dynamin-like guanosine triphosphatase OPA1 as a result of suppressed FA utilization. Enhancing FA utilization upregulated YME1L expression and subsequently rebalanced OPA1 processing, resulting in restoration of mitochondrial morphology in the failing heart. In addition, cardiac-specific overexpression of YME1L exerted similar cardioprotective effects against HF to those provided by HFD or CD36 overexpression. Conclusions: These findings demonstrate that enhancing FA utilization ameliorates mitochondrial fragmentation and cardiac dysfunction via rebalancing OPA1 processing in pressure overload-induced HF, suggesting a unique metabolic intervention approach to improving cardiac functions in HF.
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