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

7 results

SS31 Alleviates Pressure Overload-Induced Heart Failure Caused by Sirt3-Mediated Mitochondrial Fusion.

Suo M, Qi Y, Liu L, Zhang C, Li J, Yan X, Zhang C, Ti Y, Chen T, Bu P

Frontiers in cardiovascular medicine3 May 2022Cited by 18 (Europe PMC)

PMID35592397 (opens in a new tab)PMCIDPMC9110818 (opens in a new tab)DOI10.3389/fcvm.2022.858594 (opens in a new tab)PepBankPUB-35592397
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Summary

Heart failure caused by pressure overload is one of the leading causes of heart failure worldwide, but its pathological origin remains poorly understood. It remains critical to discover and find new improvements and treatments for pressure overload-induced heart failure. According to previous studies, mitochondrial dysfunction and myocardial interstitial fibrosis are important mechanisms for the development of heart failure. The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane. Whether SS31 alleviates pressure overload-induced heart failure through the regulation of mitochondrial fusion has not yet been confirmed. We established a pressure-overloaded heart failure mouse model through TAC surgery and found that SS31 can significantly improve cardiac function, reduce myocardial interstitial fibrosis, and increase the expression of optic atrophy-associated protein 1 (OPA1), a key protein in mitochondrial fusion. Interestingly, the role of SS31 in improving heart failure and reducing fibrosis is inseparable from the presence of sirtuin3 (Sirt3). We found that in Sirt3KO mice and fibroblasts, the effects of SS31 on improving heart failure and improving fibroblast transdifferentiation were disappeared. Likewise, Sirt3 has direct interactions with proteins critical for mitochondrial fission and fusion. We found that SS31 failed to increase OPA1 expression in both Sirt3KO mice and fibroblasts. Thus, SS31 can alleviate pressure overload-induced heart failure through Sirt3-mediated mitochondrial fusion. This study provides new directions and drug options for the clinical treatment of heart failure caused by pressure overload.
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 after TAC surgery, SS31 significantly improved cardiac function.

    In plain wordsIn mice with heart failure from pressure overload, SS31 improved heart function.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseCardiac function
    Study

    mousen: not reported in source

    TAC pressure-overload heart failure mouse model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We established a pressure-overloaded heart failure mouse model through TAC surgery and found that SS31 can significantly improve cardiac function, reduce myocardial interstitial fibrosis, and increase the expression of optic atrophy-associated protein 1 (OPA1), a key protein in mitochondrial fusion.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with pressure-overload heart failure after TAC surgery, SS31 reduced myocardial interstitial fibrosis.

    In plain wordsIn mice with heart failure from pressure overload, SS31 reduced scarring in heart tissue.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMyocardial interstitial fibrosis
    Study

    mousen: not reported in source

    TAC pressure-overload heart failure mouse model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We established a pressure-overloaded heart failure mouse model through TAC surgery and found that SS31 can significantly improve cardiac function, reduce myocardial interstitial fibrosis, and increase the expression of optic atrophy-associated protein 1 (OPA1), a key protein in mitochondrial fusion.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with pressure-overload heart failure after TAC surgery, SS31 increased expression of OPA1, a key protein in mitochondrial fusion.

    In plain wordsIn mice with heart failure from pressure overload, SS31 raised levels of OPA1, a protein for mitochondrial fusion.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseOPA1 expression
    Study

    mousen: not reported in source

    TAC pressure-overload heart failure mouse model
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We established a pressure-overloaded heart failure mouse model through TAC surgery and found that SS31 can significantly improve cardiac function, reduce myocardial interstitial fibrosis, and increase the expression of optic atrophy-associated protein 1 (OPA1), a key protein in mitochondrial fusion.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In Sirt3KO mice, the effect of SS31 on improving heart failure disappeared.

    In plain wordsIn mice lacking Sirt3, SS31 no longer improved heart failure.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeHeart failure improvement in Sirt3KO mice
    Study

    mousen: not reported in source

    Sirt3KO mice with TAC
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that in Sirt3KO mice and fibroblasts, the effects of SS31 on improving heart failure and improving fibroblast transdifferentiation were disappeared.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In Sirt3KO mice, SS31 failed to increase OPA1 expression.

    In plain wordsIn mice lacking Sirt3, SS31 did not raise OPA1 levels.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeOPA1 expression in Sirt3KO mice
    Study

    mousen: not reported in source

    Sirt3KO mice with TAC
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that SS31 failed to increase OPA1 expression in both Sirt3KO mice and fibroblasts.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  6. 06LabIn vitro (cells)Mechanism

    In Sirt3KO fibroblasts, the effect of SS31 on improving fibroblast transdifferentiation disappeared.

    In plain wordsIn cells lacking Sirt3, SS31 no longer improved fibroblast transformation.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeFibroblast transdifferentiation in Sirt3KO fibroblasts
    Study

    n: not reported in source

    Sirt3KO fibroblasts
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that in Sirt3KO mice and fibroblasts, the effects of SS31 on improving heart failure and improving fibroblast transdifferentiation were disappeared.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.
  7. 07LabIn vitro (cells)Mechanism

    In Sirt3KO fibroblasts, SS31 failed to increase OPA1 expression.

    In plain wordsIn cells lacking Sirt3, SS31 did not raise OPA1 levels.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeOPA1 expression in Sirt3KO fibroblasts
    Study

    n: not reported in source

    Sirt3KO fibroblasts
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that SS31 failed to increase OPA1 expression in both Sirt3KO mice and fibroblasts.
    1 context sentence
    Summary · context
    The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane.

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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