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Study · Animal study (in vivo) · mouse · 2026

7 results

Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis.

Dong W, Zhang W, Huang L, Xiao L, Luo Y, Yuan L, Jiang Y, Liao A, Zhao H, Liu Z, Wang J, Zhao Y and 6 more

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Cai Y, Peng M, Yang D, Xie Y, Li K, Zhu W

Journal of advanced research12 Mar 2026

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 study7

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice with cerebral ischemia-reperfusion injury, SS‑31 inhibited cardiolipin release.

    In plain wordsIn mice with stroke-like injury, SS‑31 reduced the release of cardiolipin from cells.

    Outcome
    DecreaseCardiolipin release
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 inhibits CL release, preserves CL content, and subsequently restores CL homeostasis.
    1 context sentence
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with cerebral ischemia-reperfusion injury, SS‑31 preserved cardiolipin content.

    In plain wordsIn mice with stroke-like injury, SS‑31 helped keep cardiolipin levels in brain tissue.

    Outcome
    IncreaseCardiolipin content
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 inhibits CL release, preserves CL content, and subsequently restores CL homeostasis.
    1 context sentence
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with cerebral ischemia-reperfusion injury, SS‑31 restored cardiolipin homeostasis.

    In plain wordsIn mice with stroke-like injury, SS‑31 restored the normal balance of cardiolipin.

    Outcome
    IncreaseCardiolipin homeostasis
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 inhibits CL release, preserves CL content, and subsequently restores CL homeostasis.
    1 context sentence
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice, restoring cardiolipin homeostasis with SS‑31 attenuated cerebral ischemia-reperfusion injury.

    In plain wordsIn mice with stroke-like injury, SS‑31 restored cardiolipin balance, and brain injury was less severe.

    Outcome
    DecreaseCerebral ischemia-reperfusion injury
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Restoring CL homeostasis attenuated cerebral I/R injury by suppressing neuronal ferroptosis.
    2 context sentences
    Summary · context
    SS-31 mitigates I/R injury by restoring CL homeostasis and ameliorating ATG5-mediated autophagy-dependent neuronal ferroptosis, offering a novel therapeutic avenue for stroke.
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice, restoring cardiolipin homeostasis with SS‑31 suppressed neuronal ferroptosis.

    In plain wordsIn mice with stroke-like injury, SS‑31 restored cardiolipin balance and reduced a form of nerve cell death called ferroptosis.

    Outcome
    DecreaseNeuronal ferroptosis
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Restoring CL homeostasis attenuated cerebral I/R injury by suppressing neuronal ferroptosis.
    2 context sentences
    Summary · context
    ameliorating ATG5-mediated autophagy-dependent neuronal ferroptosis, offering a novel therapeutic avenue for stroke.
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  6. 06AnimalAnimal study (in vivo)Mechanism

    SS‑31 downregulated autophagy-associated genes, with ATG5 identified as the crucial target.

    In plain wordsIn mice with stroke-like injury, SS‑31 lowered activity of autophagy genes, with ATG5 as the key target.

    Outcome
    DecreaseAutophagy-associated gene expression, ATG5
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, SS-31 downregulated autophagy-associated genes, with ATG5 identified as the crucial target.
    1 context sentence
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
  7. 07AnimalAnimal study (in vivo)Mechanism

    Activating autophagy or overexpressing ATG5 reversed the protective effects of SS‑31.

    In plain wordsIn mice with stroke-like injury, switching on autophagy or raising ATG5 undid the protection that SS‑31 gave.

    Outcome
    Not applicableReversal of SS-31 protection by autophagy activation or ATG5 overexpression
    Study

    mousen: not reported in source

    MCAO/R cerebral ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Activating autophagy or overexpressing ATG5 reversed the protective effects of SS-31.
    1 context sentence
    Summary · context
    Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.

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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