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Study · Animal study (in vivo) · 2013

5 results

Global proteomics and pathway analysis of pressure-overload-induced heart failure and its attenuation by mitochondrial-targeted peptides.

Dai DF, Hsieh EJ, Chen T, Menendez LG, Basisty NB, Tsai L, Beyer RP, Crispin DA, Shulman NJ, Szeto HH, Tian R, MacCoss MJ, Rabinovitch PS

Circulation. Heart failure9 Aug 2013Cited by 124 (Europe PMC)

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 study5

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In the TAC heart failure model, concomitant SS31 ameliorated the congestive heart failure phenotypes.

    In plain wordsIn animals with pressure-overload heart failure, SS31 given at the same time reduced signs of heart failure.

    Outcome
    DecreaseCongestive heart failure phenotypes after TAC
    Study

    n: not reported in source

    Transverse aortic constriction (TAC) heart failure
    Comparator
    TAC without SS31
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Concomitant treatment with SS31 ameliorated the congestive heart failure phenotypes and mitochondrial damage induced by TAC
    1 context sentence
    Summary · context
    We applied an improved label-free shotgun proteomics approach to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the associated signaling pathway changes using ingenuity pathway analysis.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In the TAC heart failure model, concomitant SS31 ameliorated mitochondrial damage.

    In plain wordsIn animals with pressure-overload heart failure, SS31 given at the same time reduced damage to heart mitochondria.

    Outcome
    DecreaseMitochondrial damage after TAC
    Study

    n: not reported in source

    Transverse aortic constriction (TAC) heart failure
    Comparator
    TAC without SS31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Concomitant treatment with SS31 ameliorated the congestive heart failure phenotypes and mitochondrial damage induced by TAC
    1 context sentence
    Summary · context
    We applied an improved label-free shotgun proteomics approach to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the associated signaling pathway changes using ingenuity pathway analysis.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In the TAC heart failure model, SS31 attenuated TAC-induced mitochondrial proteome changes, with an average of 84% protection.

    In plain wordsIn animals with pressure-overload heart failure, SS31 prevented about 84% of the changes in mitochondrial proteins.

    Outcome
    DecreaseMitochondrial proteome changes after TAC
    Study

    n: not reported in source

    Transverse aortic constriction (TAC) heart failure
    Comparator
    TAC without SS31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    Protection of mitochondrial protein changes (average)
    84%
    SS31 with TAC

    Source sentences

    Summary
    Concomitant treatment with SS31 ameliorated the congestive heart failure phenotypes and mitochondrial damage induced by TAC, in parallel with global attenuation of mitochondrial proteome changes, with an average of 84% protection of mitochondrial and 69% of nonmitochondrial protein changes.
    1 context sentence
    Summary · context
    We applied an improved label-free shotgun proteomics approach to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the associated signaling pathway changes using ingenuity pathway analysis.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In the TAC heart failure model, SS31 attenuated TAC-induced non-mitochondrial protein changes, with an average of 69% protection.

    In plain wordsIn animals with pressure-overload heart failure, SS31 prevented about 69% of the changes in non-mitochondrial proteins.

    Outcome
    DecreaseNon-mitochondrial proteome changes after TAC
    Study

    n: not reported in source

    Transverse aortic constriction (TAC) heart failure
    Comparator
    TAC without SS31
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    Protection of non-mitochondrial protein changes (average)
    69%
    SS31 with TAC

    Source sentences

    Summary
    Concomitant treatment with SS31 ameliorated the congestive heart failure phenotypes and mitochondrial damage induced by TAC, in parallel with global attenuation of mitochondrial proteome changes, with an average of 84% protection of mitochondrial and 69% of nonmitochondrial protein changes.
    1 context sentence
    Summary · context
    We applied an improved label-free shotgun proteomics approach to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the associated signaling pathway changes using ingenuity pathway analysis.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In the TAC heart failure model, SS31 significantly ameliorated the changes in all the TAC-affected pathways identified by ingenuity pathway analysis.

    In plain wordsIn animals with pressure-overload heart failure, SS31 significantly reduced changes in all the affected protein pathways.

    Outcome
    DecreaseSignaling pathway changes after TAC
    Study

    n: not reported in source

    Transverse aortic constriction (TAC) heart failure
    Comparator
    TAC without SS31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This included significant amelioration of all the ingenuity pathway analysis noted above.
    1 context sentence
    Summary · context
    We applied an improved label-free shotgun proteomics approach to evaluate the global proteomics changes in transverse aortic constriction (TAC)-induced heart failure and the associated signaling pathway changes using ingenuity pathway analysis.

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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