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

9 results

A mitochondrial-targeted peptide ameliorated podocyte apoptosis through a HOCl-alb-enhanced and mitochondria-dependent signalling pathway in diabetic rats and in vitro.

Wang X, Tang D, Zou Y, Wu X, Chen Y, Li H, Chen S, Shi Y, Niu H

Journal of enzyme inhibition and medicinal chemistry1 Dec 2019Cited by 27 (Europe PMC)

PMID30734599 (opens in a new tab)PMCIDPMC6327984 (opens in a new tab)DOI10.1080/14756366.2018.1488697 (opens in a new tab)PepBankPUB-30734599
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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: CC BY-NC. Results still quote short attributed sentences.

Results from this study9

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented the reduction in glomerular podocyte number.

    In plain wordsIn diabetic rats, SS‑31 prevented the loss of kidney podocyte cells caused by a damaging albumin challenge.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseGlomerular podocyte number
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Comparator
    HOCl-alb challenge without SS-31
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Compared with the control group, the glomerular podocyte number and expression of WT1 were significantly reduced and TUNEL-positive podocytes were significantly increased in renal tissues in the diabetic rat. These effects were further exacerbated by hypochlorite-modified albumin (HOCl-alb) challeng…
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented the reduction in WT1 expression.

    In plain wordsIn diabetic rats, SS‑31 prevented the drop in a kidney podocyte marker caused by a damaging albumin challenge.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseWT1 expression in podocytes
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Comparator
    HOCl-alb challenge without SS-31
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Compared with the control group, the glomerular podocyte number and expression of WT1 were significantly reduced and TUNEL-positive podocytes were significantly increased in renal tissues in the diabetic rat. These effects were further exacerbated by hypochlorite-modified albumin (HOCl-alb) challeng…
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented the increase in TUNEL-positive podocytes.

    In plain wordsIn diabetic rats, SS‑31 prevented the rise in dying podocyte cells caused by a damaging albumin challenge.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseTUNEL-positive podocytes
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Comparator
    HOCl-alb challenge without SS-31
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Compared with the control group, the glomerular podocyte number and expression of WT1 were significantly reduced and TUNEL-positive podocytes were significantly increased in renal tissues in the diabetic rat. These effects were further exacerbated by hypochlorite-modified albumin (HOCl-alb) challeng…
  4. 04AnimalAnimal study (in vivo)Mechanism

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented oxidative stress.

    In plain wordsIn diabetic rats, SS‑31 prevented oxidative stress caused by a damaging albumin challenge.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseOxidative stress by HOCl-alb in vivo
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro
  5. 05AnimalAnimal study (in vivo)Mechanism

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented mitochondria-dependent apoptosis signalling, shown by reduced cytochrome c release.

    In plain wordsIn diabetic rats, SS‑31 prevented a mitochondrial cell-death signal, shown by less cytochrome c release.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCytochrome c release
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented mitochondria-dependent apoptosis signalling, shown by reduced Apaf-1 binding to caspase-9.

    In plain wordsIn diabetic rats, SS‑31 prevented a mitochondrial cell-death signal, shown by less Apaf-1 and caspase-9 binding.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseApaf-1 and caspase-9 binding
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In diabetic rats challenged with HOCl-alb, SS‑31 prevented mitochondria-dependent apoptosis signalling, shown by reduced caspase activation.

    In plain wordsIn diabetic rats, SS‑31 prevented a mitochondrial cell-death signal, shown by less caspase activation.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCaspase activation
    Study

    ratn: not reported in source

    Diabetic rats challenged with HOCl-alb
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.
  8. 08LabIn vitro (cells)Efficacy outcome

    In a podocyte cell line, SS‑31 blocked apoptosis induced by HOCl-alb.

    In plain wordsIn podocyte cells in the lab, SS‑31 blocked cell death caused by a damaging albumin.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseHOCl-alb-induced podocyte apoptosis in vitro
    Study

    n: not reported in source

    Podocyte cell line
    Comparator
    HOCl-alb without SS-31
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, SS-31 blocked apoptosis in podocyte cell line induced by HOCl-alb.
  9. 09LabIn vitro (cells)Mechanism

    In a podocyte cell line, SS‑31 prevented oxidative stress and mitochondria-dependent apoptosis signalling induced by HOCl-alb.

    In plain wordsIn podocyte cells in the lab, SS‑31 prevented oxidative stress and a mitochondrial cell-death signal caused by a damaging albumin.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseOxidative stress and mitochondria-dependent apoptosis signalling in vitro
    Study

    n: not reported in source

    Podocyte cell line
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.
    1 context sentence
    Summary · context
    In vitro, SS-31 blocked apoptosis in podocyte cell line induced by HOCl-alb.

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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