ArticleeLife2020
Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
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Who cites it
82 citing papers in PubMed, 125 citations in OpenAlex.
- Article
- Mitochondrial-targeted SS-31 peptide attenuates radiation-induced cardiomyocyte senescence.Journal of radiation research · 2026Article
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence.Biology · 2026Article
- Heart failure in the elderly: epidemiology, mechanisms, and management.European heart journal · 2026Review
- Low-Level Domoic Acid Exposure Induces Age-like Cardiomyopathy in Young Adult and Aged Mice.Marine drugs · 2026Article
- Nanoparticles in Vascular Dementia: Advantages and Challenges.CNS neuroscience & therapeutics · 2026Review
- TCONS_00052110 is associated with prolonged PTBP1 half-life and mitochondrial injury in PAH-associated right ventricular stress.Scientific reports · 2026Article
- Mitoregulin supports mitochondrial membrane integrity and protects against cardiac ischaemia-reperfusion injury.Cardiovascular research · 2026Article
- Research advances and application prospects of CAR-T therapy in the treatment of age-related diseases.Frontiers in immunology · 2026Review
- From Earth to orbit: cardiovascular innovation diffusion to space medicine - an updated review incorporating a novel predictive modeling framework.Frontiers in physiology · 2026Article
- Succinate-driven PKM2 succinylation and dimerization accelerates age-associated cardiac fibrosis.Communications biology · 2025Article
- Diabetic cardiomyopathy: Mechanistic insights on molecular pathways and emerging therapeutic approaches.Heart failure reviews · 2025Review
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Mitochondrial Dynamics in Aging Heart.Biomedicines · 2025Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- The effect of enhanced glycolysis on cardiac aging.GeroScience · 2025Article
- The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances.Biology · 2025Review
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Mitochondrial-Targeted Protective Potential of Elamipretide for the In Vitro Production of Porcine Embryos.Animals : an open access journal from MDPI · 2025Article
- Roadmap for alleviating the manifestations of ageing in the cardiovascular system.Nature reviews. Cardiology · 2025Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 1 country.
Funding
Abstract
Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochondrial ROS in cardiomyocytes from old mice, accompanied by reduced protein oxidation and a shift towards a more reduced protein thiol redox state in old hearts. Improved diastolic function was concordant with increased phosphorylation of cMyBP-C Ser282 but was independent of titin isoform shift. Late-life viral expression of mitochondrial-targeted catalase (mCAT) produced similar functional benefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizing mitochondrial oxidative stress as an overlapping mechanism. These results demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial energetics and redox signaling as therapeutic targets for cardiac aging.
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What OpenQuestion holds
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.