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Study · Ex vivo tissue · rat · 2026

6 results

MOTS-c preserves mitochondrial subpopulation bioenergetics and genome integrity to attenuate cardiac ischemia reperfusion injury.

Santhanam SS, Jayaraman S, Rajesh SS, Iyer VNH, Kurian GA

Molecular biology reports2 Jun 2026

PMID42228044 (opens in a new tab)DOI10.1007/s11033-026-12064-7 (opens in a new tab)PepBankPUB-42228044
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

6 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabEx vivo tissueEfficacy outcome

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment improved post-ischemic mechanical recovery.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c improved how well the heart pumped again.

    Peptide
    MOTS-c
    Outcome
    IncreasePost-ischemic mechanical recovery
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    MOTS-c treatment improved post-ischemic mechanical recovery
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.
  2. 02LabEx vivo tissueMechanism

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment attenuated oxidative stress.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c reduced oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress after ischemia-reperfusion
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    attenuated oxidative stress
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.
  3. 03LabEx vivo tissueMechanism

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment partially preserved mitochondrial enzyme activities.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c partly kept mitochondrial enzyme activity.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial enzyme activities
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    partially preserved mitochondrial enzyme activities and membrane potential, and mitigated reductions in mtDNA copy number and mitochondrial gene expression.
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.
  4. 04LabEx vivo tissueMechanism

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment partially preserved mitochondrial membrane potential.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c partly kept the mitochondrial membrane potential.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial membrane potential
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    partially preserved mitochondrial enzyme activities and membrane potential, and mitigated reductions in mtDNA copy number and mitochondrial gene expression.
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.
  5. 05LabEx vivo tissueMechanism

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment mitigated the reduction in mtDNA copy number.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c lessened the loss of mitochondrial DNA copies.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial DNA copy number
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    mitigated reductions in mtDNA copy number and mitochondrial gene expression.
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.
  6. 06LabEx vivo tissueMechanism

    In isolated rat hearts after ischemia-reperfusion, MOTS‑c treatment mitigated the reduction in mitochondrial gene expression.

    In plain wordsIn isolated rat hearts after a blocked blood flow injury, MOTS‑c lessened the drop in mitochondrial gene activity.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial gene expression
    Study

    ratn = 6

    Langendorff-perfused isolated heart, ischemia-reperfusion
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    53 µMAs given in this study (rat).

    Source sentences

    Summary
    mitigated reductions in mtDNA copy number and mitochondrial gene expression.
    2 context sentences
    Summary · context
    Isolated female Wistar rat hearts (n = 6/group) were subjected to 30 min global ischemia followed by 60 min reperfusion using the Langendorff perfusion model.
    Summary · context
    MOTS-c (53 µM) was administered either before ischemia or at reperfusion onset.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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