ReviewHeart failure reviews2013
Alterations in mitochondrial function in cardiac hypertrophy and heart failure.
Review in Heart failure reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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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.
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Who cites it
38 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Mitochondria-resident SBK3 confers protection against pressure overload-induced heart failure in mice.Acta biochimica et biophysica Sinica · 2025Article
- SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism.Scientific reports · 2025Article
- Decoding glycosylation in cardiovascular diseases: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Cinnamic acid alleviates hypertensive left ventricular hypertrophy by antagonizing the vasopressor activity and the pro-cardiac hypertrophic signaling of angiotensin II.Frontiers in pharmacology · 2025Article
- Evidence for enduring cardiac and multiorgan toxicity after repeated exposure to the synthetic cannabinoid JWH-018 in male rats.Toxicology · 2024Article
- Hyperbaric oxygen treatment reveals spatiotemporal OXPHOS plasticity in the porcine heart.PNAS nexus · 2024Article
- Transcriptome analysis of human hypertrophic cardiomyopathy reveals inhibited cardiac development pathways in children.iScience · 2024Article
- Multimodal ultrasound imaging of a rat model with ischemic heart failure and its relationship to histopathology.American journal of translational research · 2024Article
- Inhibition of MEG3 ameliorates cardiomyocyte apoptosis and autophagy by regulating the expression of miRNA-129-5p in a mouse model of heart failure.Redox report : communications in free radical research · 2023Article
- Status of Mitochondrial Oxidative Phosphorylation during the Development of Heart Failure.Antioxidants (Basel, Switzerland) · 2023Review
- Targeting Mitochondrial Metabolism to Save the Failing Heart.Life (Basel, Switzerland) · 2023Review
- Metformin Collaborates with PINK1/Mfn2 Overexpression to Prevent Cardiac Injury by Improving Mitochondrial Function.Biology · 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
- Myocardial capacity of mitochondrial oxidative phosphorylation in response to prolonged electromagnetic stress.Frontiers in cardiovascular medicine · 2023Article
- Small-molecule 7,8-dihydroxyflavone counteracts compensated and decompensated cardiac hypertrophy via AMPK activation.Journal of geriatric cardiology : JGC · 2022Article
- A New Minimally Invasive Method of Transverse Aortic Constriction in Mice.Journal of cardiovascular translational research · 2022Article
- Proteomic mapping of atrial and ventricular heart tissue in patients with aortic valve stenosis.Scientific reports · 2021Article
- Therapeutic potential and recent advances on targeting mitochondrial dynamics in cardiac hypertrophy: A concise review.Molecular therapy. Nucleic acids · 2021Review
- Between Inflammation and Autophagy: The Role of Leptin-Adiponectin Axis in Cardiac Remodeling.Journal of inflammation research · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal cardiac function requires high and continuous supply with ATP. As mitochondria are the major source of ATP production, it is apparent that mitochondrial function and cardiac function need to be closely related to each other. When subjected to overload, the heart hypertrophies. Initially, the development of hypertrophy is a compensatory mechanism, and contractile function is maintained. However, when the heart is excessively and/or persistently stressed, cardiac function may deteriorate, leading to the onset of heart failure. There is considerable evidence that alterations in mitochondrial function are involved in the decompensation of cardiac hypertrophy. Here, we review metabolic changes occurring at the mitochondrial level during the development of cardiac hypertrophy and the transition to heart failure. We will focus on changes in mitochondrial substrate metabolism, the electron transport chain and the role of oxidative stress. We will demonstrate that, with respect to mitochondrial adaptations, a clear distinction between hypertrophy and heart failure cannot be made because most of the findings present in overt heart failure can already be found in the various stages of hypertrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.