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Study · Animal study (in vivo) · 2026

4 results

Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-β signaling pathway.

Li Z, Wang T, Fu Y, Chen F, Li S

Frontiers in endocrinology3 Feb 2026Cited by 1 (Europe PMC)

PMID41710402 (opens in a new tab)PMCIDPMC12909204 (opens in a new tab)DOI10.3389/fendo.2026.1732329 (opens in a new tab)PepBankPUB-41710402
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Summary

Myocardial fibrosis stands as a defining pathological characteristic in type 2 diabetes. Aerobic exercise curbs the overproduction of type I/III collagen and boosts matrix metalloproteinases, thereby improving outcomes related to fibrosis in the heart. Although physical activity is well known for its positive effects on cardiac well-being in diabetic individuals, sticking to an exercise regimen proves to be a tough nut to crack for many patients. The mitochondrial peptide MOTS-c could serve as a stand-in for exercise, delivering cardioprotective benefits akin to those from working out. This study delved into the molecular mechanisms behind how exercise and MOTS-c influence cardiac fibrosis in diabetes. Both approaches led to marked enhancements in glucose and lipid metabolism, lowered collagen buildup, and bettered both systolic and diastolic heart functions. Through transcriptomic profiling, THBS1 emerged as a pivotal gene that was altered, with reduced activity in the THBS1/TGF-β pathway verified at mRNA and protein stages. In a nutshell, these insights indicate that aerobic exercise and MOTS-c alleviate myocardial fibrosis in diabetes, most likely by putting a damper on the THBS1/TGF-β signaling pathway. These findings establish a theoretical foundation for treating diabetic myocardial fibrosis.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In a diabetic myocardial fibrosis model, MOTS‑c markedly improved glucose and lipid metabolism.

    In plain wordsIn diabetic animals, MOTS‑c improved sugar and fat metabolism.

    Peptide
    MOTS-c
    Outcome
    Direction not reportedGlucose and lipid metabolism
    Study

    n: not reported in source

    Diabetic myocardial fibrosis model
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both approaches led to marked enhancements in glucose and lipid metabolism, lowered collagen buildup, and bettered both systolic and diastolic heart functions.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a diabetic myocardial fibrosis model, MOTS‑c lowered collagen buildup.

    In plain wordsIn diabetic animals, MOTS‑c reduced collagen buildup in the heart.

    Peptide
    MOTS-c
    Outcome
    DecreaseCollagen deposition in the heart
    Study

    n: not reported in source

    Diabetic myocardial fibrosis model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both approaches led to marked enhancements in glucose and lipid metabolism, lowered collagen buildup, and bettered both systolic and diastolic heart functions.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In a diabetic myocardial fibrosis model, MOTS‑c improved systolic and diastolic heart function.

    In plain wordsIn diabetic animals, MOTS‑c improved how well the heart contracts and relaxes.

    Peptide
    MOTS-c
    Outcome
    IncreaseSystolic and diastolic heart function
    Study

    n: not reported in source

    Diabetic myocardial fibrosis model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both approaches led to marked enhancements in glucose and lipid metabolism, lowered collagen buildup, and bettered both systolic and diastolic heart functions.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In a diabetic myocardial fibrosis model, MOTS‑c was linked to reduced THBS1/TGF-β pathway activity, verified at mRNA and protein level.

    In plain wordsIn diabetic animals, MOTS‑c was linked to lower activity of the THBS1/TGF-β signalling pathway, which is linked to heart scarring.

    Peptide
    MOTS-c
    Outcome
    DecreaseTHBS1/TGF-β signaling pathway activity
    Study

    n: not reported in source

    Diabetic myocardial fibrosis model
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Through transcriptomic profiling, THBS1 emerged as a pivotal gene that was altered, with reduced activity in the THBS1/TGF-β pathway verified at mRNA and protein stages.
    1 context sentence
    Summary · context
    In a nutshell, these insights indicate that aerobic exercise and MOTS-c alleviate myocardial fibrosis in diabetes, most likely by putting a damper on the THBS1/TGF-β signaling pathway.

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

    10 Oct 2026, 08:19 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.

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