ReviewJournal of clinical medicine2020
Mitochondrial Pathobiology and Metabolic Remodeling in Progression to Overt Systolic Heart Failure.
Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2026Article
- Gene Therapy for Heart Failure: Impact on Mitochondrial Dysfunction.Biomedicines · 2026Review
- Gut-derived metabolites and mitochondrial homeostasis in heart failure: mechanistic links and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.Biomolecules · 2024Review
- Cardiometabolic Changes in Sirtuin1-Heterozygous Mice on High-Fat Diet and Melatonin Supplementation.International journal of molecular sciences · 2024Article
- Multi-Omics Profiling of Hypertrophic Cardiomyopathy Reveals Altered Mechanisms in Mitochondrial Dynamics and Excitation-Contraction Coupling.International journal of molecular sciences · 2023Article
- Rg3 regulates myocardial pyruvate metabolism via P300-mediated dihydrolipoamide dehydrogenase 2-hydroxyisobutyrylation in TAC-induced cardiac hypertrophy.Cell death & disease · 2022Article
- Review
- Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy.Experimental and therapeutic medicine · 2022Article
- Reactive Oxygen Species Induced Pathways in Heart Failure Pathogenesis and Potential Therapeutic Strategies.Biomedicines · 2022Review
- Human myocardial mitochondrial oxidative capacity is impaired in mild acute heart transplant rejection.ESC heart failure · 2021Article
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
- Physical Exercise: A Novel Tool to Protect Mitochondrial Health.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The mitochondria are mostly abundant in the heart, a beating organ of high- energy demands. Their function extends beyond being a power plant of the cell including redox balance, ion homeostasis and metabolism. They are dynamic organelles that are tethered to neighboring structures, especially the endoplasmic reticulum. Together, they constitute a functional unit implicated in complex physiological and pathophysiological processes. Their topology in the cell, the cardiac myocyte in particular, places them at the hub of signaling and calcium homeostasis, making them master regulators of cell survival or cell death. Perturbations in mitochondrial function play a central role in the pathophysiology of myocardial remodeling and progression of heart failure. In this minireview, we summarize important pathophysiological mechanisms, pertaining to mitochondrial morphology, dynamics and function, which take place in compensated hypertrophy and in progression to overt systolic heart failure. Published work in the last few years has expanded our understanding of these important mechanisms; a key prerequisite to identifying therapeutic strategies targeting mitochondrial dysfunction in heart failure.
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Registered trials
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