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Study · Animal study (in vivo) · mouse · 2019

5 results

Differential Effects of the Mitochondria-Active Tetrapeptide SS-31 (D-Arg-dimethylTyr-Lys-Phe-NH2) and Its Peptidase-Targeted Prodrugs in Experimental Acute Kidney Injury.

Wyss JC, Kumar R, Mikulic J, Schneider M, Mary JL, Aebi JD, Juillerat-Jeanneret L, Golshayan D, Golshayan D

Frontiers in pharmacology8 Nov 2019Cited by 14 (Europe PMC)

PMID31780923 (opens in a new tab)PMCIDPMC6857474 (opens in a new tab)DOI10.3389/fphar.2019.01209 (opens in a new tab)PepBankPUB-31780923
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Summary

The mitochondria-active tetrapeptide SS-31 can control oxidative tissue damage in kidney diseases. To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed. Reduction of acute kidney injury was demonstrated in mice treated with SS-31. The expression of mRNAs involved in acute inflammatory and oxidative stress responses in the diseased kidneys confirmed that SS-31 could regulate these pathways in our in vivo models. Furthermore, ex vivo histoenzymography of mouse kidneys showed that aminopeptidase A (APA), the enzyme involved in the processing of angiotensin (Ang) II to Ang III, was induced in the diseased kidneys, and its activity was inhibited by SS-31. As the renin-angiotensin system (RAS) is a main regulator of kidney functions, the modulation of Ang receptors (ATR) and APA by SS-31 was further investigated using mRNAs extracted from diseased kidneys. Following acute tubular and/or glomerular damage, the expression of the AT1R mRNA was upregulated, which could be selectively downregulated upon SS-31 administration to the animals. At the same time, SS-31 was able to increase the expression of the AT2R, which may contribute to limit renal damage. Consequently, SS-31-based prodrugs were developed as substrates and/or inhibitors for APA and were screened using cells expressing high levels of APA, showing its selective regulation by α-Glu-SS-31. Thus, a link between SS-31 and the RAS opens new therapeutic implications for SS-31 in kidney diseases.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

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 mice with experimental acute kidney injury, SS‑31 reduced the kidney injury.

    In plain wordsIn mice with kidney injury, SS‑31 reduced the injury.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAcute kidney injury
    Study

    mousen: not reported in source

    Murine models of acute tubular injury and glomerular damage
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Reduction of acute kidney injury was demonstrated in mice treated with SS-31.
    1 context sentence
    Summary · context
    To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with acute kidney injury, SS‑31 regulated the expression of mRNAs involved in acute inflammatory and oxidative stress responses.

    In plain wordsIn mice with kidney injury, SS‑31 changed the activity of genes linked to inflammation and oxidative stress.

    Peptide
    Elamipretide (SS-31)
    Outcome
    MixedInflammatory and oxidative stress response mRNAs in injured kidney
    Study

    mousen: not reported in source

    Murine models of acute tubular injury and glomerular damage
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The expression of mRNAs involved in acute inflammatory and oxidative stress responses in the diseased kidneys confirmed that SS-31 could regulate these pathways in our in vivo models.
    1 context sentence
    Summary · context
    To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mouse kidneys with acute injury, SS‑31 inhibited the induced aminopeptidase A activity.

    In plain wordsIn mice with kidney injury, SS‑31 reduced the activity of an enzyme (aminopeptidase A) that was raised in the diseased kidney.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAminopeptidase A activity in diseased kidney
    Study

    mousen: not reported in source

    Murine models of acute tubular injury and glomerular damage
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, ex vivo histoenzymography of mouse kidneys showed that aminopeptidase A (APA), the enzyme involved in the processing of angiotensin (Ang) II to Ang III, was induced in the diseased kidneys, and its activity was inhibited by SS-31.
    1 context sentence
    Summary · context
    To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with acute tubular and/or glomerular damage, SS‑31 downregulated the upregulated AT1R mRNA.

    In plain wordsIn mice with kidney damage, SS‑31 lowered the raised activity of the gene for the angiotensin type 1 receptor.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAT1R mRNA expression
    Study

    mousen: not reported in source

    Murine models of acute tubular injury and glomerular damage
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Following acute tubular and/or glomerular damage, the expression of the AT1R mRNA was upregulated, which could be selectively downregulated upon SS-31 administration to the animals.
    1 context sentence
    Summary · context
    To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with acute kidney damage, SS‑31 increased AT2R expression.

    In plain wordsIn mice with kidney damage, SS‑31 raised the activity of the gene for the angiotensin type 2 receptor.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseAT2R mRNA expression
    Study

    mousen: not reported in source

    Murine models of acute tubular injury and glomerular damage
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At the same time, SS-31 was able to increase the expression of the AT2R, which may contribute to limit renal damage.
    1 context sentence
    Summary · context
    To investigate other potential beneficial nephroprotective effects of SS-31, in vivo murine models of acute tubular injury and glomerular damage were developed.

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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