ArticleMolecular biology reports2026
MOTS-c preserves mitochondrial subpopulation bioenergetics and genome integrity to attenuate cardiac ischemia reperfusion injury.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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Who cites it
1 citing paper in PubMed.
- Mitokines as bioenergetic stress signals in cardiovascular disease: mitochondrial communication, endocrine adaptation, and translational implications.Journal of bioenergetics and biomembranes · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial dysfunction contributes substantially to myocardial ischemia-reperfusion (IR) injury through impaired bioenergetics, oxidative stress, and disruption of mitochondrial homeostasis. MOTS-c, a mitochondrial-derived peptide encoded within the 12 S rRNA region of mtDNA, has been implicated in metabolic stress adaptation, although its role in myocardial IR injury remains incompletely understood. METHODS AND
resultsIsolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model. MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset. Cardiac mechanical function, myocardial injury, mitochondrial bioenergetics, oxidative stress, mtDNA copy number, and mitochondrial regulatory gene expression were evaluated in subsarcolemmal and interfibrillar mitochondrial populations. IR significantly impaired cardiac mechanical recovery, increased oxidative stress, reduced electron transport chain and dehydrogenase enzyme activities, disrupted mitochondrial membrane potential, and decreased mtDNA copy number and expression of mitochondrial regulatory genes. MOTS-c treatment improved post-ischemic mechanical recovery, attenuated oxidative stress, partially preserved mitochondrial enzyme activities and membrane potential, and mitigated reductions in mtDNA copy number and mitochondrial gene expression. Protective effects were observed in both mitochondrial subpopulations, although responses varied across parameters.
conclusionsMOTS-c treatment was associated with preservation of mitochondrial functional integrity and improved cardiac recovery following IR injury. These findings support a potential role for mitochondrial-derived peptides in modulating cardiac mitochondrial stress responses during ischemia-reperfusion injury, although the underlying signaling mechanisms require further validation.
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Registered trials
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