ArticleCell metabolism2017
Abrogating Mitochondrial Dynamics in Mouse Hearts Accelerates Mitochondrial Senescence.
Article in Cell metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
194 citing papers in PubMed, 1 synthesis or guideline pooled it, 311 citations in OpenAlex.
- Mitochondrial dysfunction in cardiovascular disease: Towards exercise regulation of mitochondrial function.Frontiers in physiology · 2023Pooled it
- Mitofusin Activation Delays Aging inCells · 2026Article
- Multiscale interactions in cardiovascular homeostasis and remodeling: from molecular coupling to organelle and multicellular networks.The journal of physiological sciences : JPS · 2026Review
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- Disrupted Mitochondrial Quality Control in Atherosclerotic Disease: Mitophagy and Dynamics in Focus.JACC. Basic to translational science · 2026Review
- RHOT Proteins Link Mitochondrial Motility to Cardiomyocyte Sarcomere Maturation.Circulation research · 2026Article
- Regulation of mitochondrial fission by Drp1 in cardiomyopathy: possible mechanisms linking cellular processes to cell death.Molecular biology reports · 2026Review
- Targeted Extracellular Vesicles Deliver Asiaticoside to Inhibit AURKB/DRP1-Mediated Mitochondrial Fission and Attenuate Hypertrophic Scar Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- The mechanism and treatment of protein acylation modification in cardiovascular disease: a narrative review.Frontiers in pharmacology · 2026Review
- Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026Review
- Targeting mitochondria to protect the heart: a matter of balance?Clinical science (London, England : 1979) · 2025Review
- Cardiac dysfunction due to mitochondrial impairment assessed by human iPS cells caused by DNM1L mutations.Pediatric research · 2025Article
- Myocardial disarray drives metabolic inefficiency in human cardiomyocytes.Communications biology · 2025Article
- Mitochondrial quality control in cardiomyocytes: safeguarding the heart against disease and ageing.Nature reviews. Cardiology · 2025Review
- Cardiac-specific overexpression of serum response factor regulates age-associated decline in mitochondrial function.GeroScience · 2025Article
- Review
- Rab14 promotes Parkin-mediated mitophagy.Molecular biology of the cell · 2025Article
- Article
- Mitochondrial ultrastructural pathology in diabetic cardiomyopathy: integrated analysis via scanning electron microscopy and 3D visualization imaging.Cardiovascular diabetology · 2025Article
134 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial fusion and fission are critical to heart health; genetically interrupting either is rapidly lethal. To understand whether it is loss of, or the imbalance between, fusion and fission that underlies observed cardiac phenotypes, we engineered mice in which Mfn-mediated fusion and Drp1-mediated fission could be concomitantly abolished. Compared to fusion-defective Mfn1/Mfn2 cardiac knockout or fission-defective Drp1 cardiac knockout mice, Mfn1/Mfn2/Drp1 cardiac triple-knockout mice survived longer and manifested a unique pathological form of cardiac hypertrophy. Over time, however, combined abrogation of fission and fusion provoked massive progressive mitochondrial accumulation that severely distorted cardiomyocyte sarcomeric architecture. Mitochondrial biogenesis was not responsible for mitochondrial superabundance, whereas mitophagy was suppressed despite impaired mitochondrial proteostasis. Similar but milder defects were observed in aged hearts. Thus, cardiomyopathies linked to dynamic imbalance between fission and fusion are temporarily mitigated by forced mitochondrial adynamism at the cost of compromising mitochondrial quantity control and accelerating mitochondrial senescence.
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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.