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Study · Animal study (in vivo) · mouse · 2011

11 results

Mitochondrial targeted antioxidant Peptide ameliorates hypertensive cardiomyopathy.

Dai DF, Chen T, Szeto H, Nieves-Cintrón M, Kutyavin V, Santana LF, Rabinovitch PS

Journal of the American College of Cardiology27 May 2011Cited by 317 (Europe PMC)

PMID21620606 (opens in a new tab)PMCIDPMC3742010 (opens in a new tab)DOI10.1016/j.jacc.2010.12.044 (opens in a new tab)PepBankPUB-21620606
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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 study11

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice given angiotensin II for 4 weeks, SS‑31 treatment did not affect the rise in systolic and diastolic blood pressure.

    In plain wordsIn mice given angiotensin II, SS‑31 did not change the rise in blood pressure.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeAngiotensin II-induced blood pressure rise
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Blood pressure · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Continuous administration of Ang for 4 weeks in mice significantly increased both systolic and diastolic blood pressure, and this was not affected by SS-31 treatment.
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-treated mice, SS‑31 substantially attenuated the up-regulation of NADPH oxidase 4.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced the rise in the oxidant-making enzyme NOX4.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseNOX4 up-regulation
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-treated mice, SS‑31 substantially attenuated mitochondrial oxidative damage.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced oxidative damage to mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial oxidative damage
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-treated mice, SS‑31 substantially attenuated the up-regulation of mitochondrial biogenesis.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced the rise in the building of new mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseUp-regulation of mitochondrial biogenesis
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-treated mice, SS‑31 substantially attenuated phosphorylation of p38 mitogen-activated protein kinase.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced the activation of the p38 stress-signal protein.

    Peptide
    Elamipretide (SS-31)
    Outcome
    Decreasep38 MAPK phosphorylation
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-treated mice, SS‑31 prevented apoptosis.

    In plain wordsIn mice given angiotensin II, SS‑31 prevented programmed cell death in the heart.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCardiac apoptosis
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apoptosis
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In angiotensin II-treated mice, SS‑31 was concomitant with amelioration of cardiac hypertrophy, despite no blood pressure-lowering effect.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced heart enlargement without lowering blood pressure.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAngiotensin II-induced cardiac hypertrophy
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apoptosis, concomitant with amelioration of Ang-induced cardiac hypertrophy
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In angiotensin II-treated mice, SS‑31 was concomitant with amelioration of diastolic dysfunction.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced problems with the heart relaxing between beats.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAngiotensin II-induced diastolic dysfunction
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apoptosis, concomitant with amelioration of Ang-induced ca…
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  9. 09AnimalAnimal study (in vivo)Efficacy outcome

    In angiotensin II-treated mice, SS‑31 was concomitant with amelioration of cardiac fibrosis.

    In plain wordsIn mice given angiotensin II, SS‑31 reduced scarring of the heart.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAngiotensin II-induced cardiac fibrosis
    Study

    mousen: not reported in source

    Angiotensin II-induced cardiomyopathy in mice
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apoptosis, concomitant with amelioration of Ang-induced ca…
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  10. 10AnimalAnimal study (in vivo)Efficacy outcome

    In Gαq overexpressing mice, 4 weeks of SS‑31 partially rescued the heart failure phenotype.

    In plain wordsIn mice with heart failure, 4 weeks of SS‑31 partly reversed the heart failure signs.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseHeart failure phenotype in Gaq overexpressing mice
    Study

    mousen: not reported in source

    Gαq overexpressing mice with heart failure
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The SS-31 administration for 4 weeks also partially rescued the heart failure phenotype of Gαq overexpressing mice.
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.
  11. 11LabIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, SS‑31 prevented angiotensin II-induced mitochondrial ROS, whereas N-acetyl cysteine did not.

    In plain wordsIn heart muscle cells, SS‑31 prevented the rise in mitochondrial reactive oxygen species caused by angiotensin II. N-acetyl cysteine did not.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAngiotensin II-induced mitochondrial ROS
    Study

    n: not reported in source

    Neonatal cardiomyocytes
    Comparator
    Angiotensin II without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ang induces mitochondrial ROS in neonatal cardiomyocytes, which is prevented by SS-31, but not the nontargeted antioxidant N-acetyl cysteine (NAC).
    1 context sentence
    Summary · context
    The mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.

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

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