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Study · Animal study (in vivo) · mouse · 2022

7 results

Mitochondrial derived peptide MOTS-c prevents the development of heart failure under pressure overload conditions in mice.

Zhong P, Peng J, Hu Y, Zhang J, Shen C

Journal of cellular and molecular medicine25 Sept 2022Cited by 30 (Europe PMC)

PMID36156853 (opens in a new tab)PMCIDPMC9639045 (opens in a new tab)DOI10.1111/jcmm.17551 (opens in a new tab)PepBankPUB-36156853
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Summary

MOTS-c, a mitochondrial-derived peptide (MDP), has been shown to have multiple biological activities such as antioxidation, anti-inflammation, and anti-apoptosis properties. In the present study, we aimed at evaluating the therapeutic effect of MOTS-c peptide in an animal model of heart failure. The heart failure mouse model was made by transverse aortic constriction (TAC) operations. The MOTS-c peptide was administrated subcutaneously by using an osmotic pump. At the end of the animal experiment, cardiac function was evaluated by echocardiography, and heart tissues were subjected to histological and molecular analysis. In vitro cultured H9C2 cells were used to test the effects of MOTS-c overexpression on cell death in response to H2 O2 stimulation. Our study showed that MOTS-c peptide attenuated TAC-induced cardiac dysfunction and remodelling. In addition, the MOTS-c peptide reduced the inflammatory response and upregulated the antioxidant capacity, coupled with the activation of the AMPK pathway in the heart of the TAC mouse model. In in vitro cultured cardiac cells, overexpression of MOTS-c was shown to activate the AMPK pathway and protect cell apoptosis in response to H2 O2 stimulation. Taken together, our study suggested that MOTS-c peptides may have therapeutic potential in treating HF.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with pressure-overload heart failure, MOTS‑c peptide attenuated TAC-induced cardiac dysfunction.

    In plain wordsIn mice with heart failure, MOTS‑c peptide lessened the loss of heart function.

    Peptide
    MOTS-c
    Outcome
    IncreaseCardiac function after TAC
    Study

    mousen: not reported in source

    Transverse aortic constriction (TAC) heart failure model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · subcutaneousAs given in this study (mouse).

    Source sentences

    Summary
    Our study showed that MOTS-c peptide attenuated TAC-induced cardiac dysfunction and remodelling.
    2 context sentences
    Summary · context
    The heart failure mouse model was made by transverse aortic constriction (TAC) operations.
    Summary · context
    The MOTS-c peptide was administrated subcutaneously by using an osmotic pump.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with pressure-overload heart failure, MOTS‑c peptide attenuated TAC-induced cardiac remodelling.

    In plain wordsIn mice with heart failure, MOTS‑c peptide lessened harmful changes in heart structure.

    Peptide
    MOTS-c
    Outcome
    DecreaseCardiac remodelling after TAC
    Study

    mousen: not reported in source

    Transverse aortic constriction (TAC) heart failure model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · subcutaneousAs given in this study (mouse).

    Source sentences

    Summary
    Our study showed that MOTS-c peptide attenuated TAC-induced cardiac dysfunction and remodelling.
    2 context sentences
    Summary · context
    The heart failure mouse model was made by transverse aortic constriction (TAC) operations.
    Summary · context
    The MOTS-c peptide was administrated subcutaneously by using an osmotic pump.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In TAC mice, MOTS‑c peptide reduced the inflammatory response in the heart.

    In plain wordsIn mice with heart failure, MOTS‑c peptide lowered inflammation in the heart.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammatory response in the heart
    Study

    mousen: not reported in source

    Transverse aortic constriction (TAC) heart failure model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated · subcutaneousAs given in this study (mouse).

    Source sentences

    Summary
    In addition, the MOTS-c peptide reduced the inflammatory response and upregulated the antioxidant capacity, coupled with the activation of the AMPK pathway in the heart of the TAC mouse model.
    2 context sentences
    Summary · context
    The heart failure mouse model was made by transverse aortic constriction (TAC) operations.
    Summary · context
    The MOTS-c peptide was administrated subcutaneously by using an osmotic pump.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In TAC mice, MOTS‑c peptide upregulated antioxidant capacity in the heart.

    In plain wordsIn mice with heart failure, MOTS‑c peptide raised antioxidant capacity in the heart.

    Peptide
    MOTS-c
    Outcome
    IncreaseAntioxidant capacity in the heart
    Study

    mousen: not reported in source

    Transverse aortic constriction (TAC) heart failure model
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated · subcutaneousAs given in this study (mouse).

    Source sentences

    Summary
    In addition, the MOTS-c peptide reduced the inflammatory response and upregulated the antioxidant capacity, coupled with the activation of the AMPK pathway in the heart of the TAC mouse model.
    2 context sentences
    Summary · context
    The heart failure mouse model was made by transverse aortic constriction (TAC) operations.
    Summary · context
    The MOTS-c peptide was administrated subcutaneously by using an osmotic pump.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In TAC mice, MOTS‑c peptide was coupled with activation of the AMPK pathway in the heart.

    In plain wordsIn mice with heart failure, MOTS‑c peptide went together with activation of the AMPK pathway in the heart.

    Peptide
    MOTS-c
    Outcome
    IncreaseAMPK pathway activation in the heart
    Study

    mousen: not reported in source

    Transverse aortic constriction (TAC) heart failure model
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated · subcutaneousAs given in this study (mouse).

    Source sentences

    Summary
    In addition, the MOTS-c peptide reduced the inflammatory response and upregulated the antioxidant capacity, coupled with the activation of the AMPK pathway in the heart of the TAC mouse model.
    2 context sentences
    Summary · context
    The heart failure mouse model was made by transverse aortic constriction (TAC) operations.
    Summary · context
    The MOTS-c peptide was administrated subcutaneously by using an osmotic pump.
  6. 06LabIn vitro (cells)Mechanism

    In cultured cardiac cells, overexpression of MOTS‑c activated the AMPK pathway.

    In plain wordsIn cells, making more MOTS‑c switched on the AMPK pathway.

    Peptide
    MOTS-c
    Outcome
    IncreaseAMPK pathway activation in cultured cardiac cells
    Study

    n: not reported in source

    Cultured H9C2 cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In in vitro cultured cardiac cells, overexpression of MOTS-c was shown to activate the AMPK pathway and protect cell apoptosis in response to H2 O2 stimulation.
    1 context sentence
    Summary · context
    In vitro cultured H9C2 cells were used to test the effects of MOTS-c overexpression on cell death in response to H2 O2 stimulation.
  7. 07LabIn vitro (cells)Efficacy outcome

    In cultured cardiac cells, overexpression of MOTS‑c protected against apoptosis caused by hydrogen peroxide.

    In plain wordsIn cells, making more MOTS‑c protected against cell death caused by hydrogen peroxide.

    Peptide
    MOTS-c
    Outcome
    DecreaseApoptosis after hydrogen peroxide stimulation
    Study

    n: not reported in source

    Cultured H9C2 cells
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In in vitro cultured cardiac cells, overexpression of MOTS-c was shown to activate the AMPK pathway and protect cell apoptosis in response to H2 O2 stimulation.
    1 context sentence
    Summary · context
    In vitro cultured H9C2 cells were used to test the effects of MOTS-c overexpression on cell death in response to H2 O2 stimulation.

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.

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