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Study · Animal study (in vivo) · mouse · 2022

2 results

SESN2 prevents the slow-to-fast myofiber shift in denervated atrophy via AMPK/PGC-1α pathway.

Yang X, Xue P, Liu Z, Li W, Li C, Chen Z, Chen Z

Cellular & molecular biology letters9 Aug 2022Cited by 19 (Europe PMC)

PMID35945510 (opens in a new tab)PMCIDPMC9361691 (opens in a new tab)DOI10.1186/s11658-022-00367-z (opens in a new tab)PepBankPUB-35945510
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Summary

BackgroundSestrin2 (SESN2), a stress-inducible protein, has been reported to protect against denervated muscle atrophy through unfolded protein response and mitophagy, while its role in myofiber type transition remains unknown.MethodsA mouse sciatic nerve transection model was created to evaluate denervated muscle atrophy. Myofiber type transition was confirmed by western blot, fluorescence staining, ATP quantification, and metabolic enzyme activity analysis. Adeno-associated virus (AAV) was adopted to achieve SESN2 knockdown and overexpression in gastrocnemius. AMPK/PGC-1α signal was detected by western blot and activated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). C2C12 myotubes with rotenone treatment were adopted for in vitro experiments.ResultsSESN2 was found to be upregulated in denervated skeletal muscles and rotenone-treated C2C12 cells. Knockdown of SESN2 aggravated muscle atrophy and accelerated myofiber type transition from slow-twitch to fast-twitch. Moreover, AMPK/PGC-1α signaling was proven to be activated by SESN2 after denervation, which further induced the expression of hypoxia-inducible factor HIF2α. Exogenous activation of AMPK/PGC-1α signaling could counteract the addition of slow-to-fast myofiber shift caused by SESN2 knockdown and lead to the retainment of muscle mass after denervation.ConclusionCollectively, the present study indicates that SESN2 prevents myofiber type transition from slow-twitch to fast-twitch and preserves muscle mass in denervated atrophy via AMPK/PGC-1α signaling. These findings contribute to a better understanding of the pathogenesis of muscle atrophy and provide novel insights into the role of SESN2 in myofiber type transition.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In denervated mice with SESN2 knockdown, exogenous AMPK/PGC-1α activation with AICAR counteracted the additional slow-to-fast myofiber shift.

    In plain wordsIn denervated mice with SESN2 knockdown, AICAR pathway activation counteracted the additional muscle fiber shift compared with knockdown alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSlow-to-fast myofiber shift
    Study

    mousen: not reported in source

    Denervated muscle with SESN2 knockdown
    Comparator
    SESN2 knockdown without exogenous pathway activation
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous activation of AMPK/PGC-1α signaling could counteract the addition of slow-to-fast myofiber shift caused by SESN2 knockdown and lead to the retainment of muscle mass after denervation.
    2 context sentences
    Summary · context
    A mouse sciatic nerve transection model was created to evaluate denervated muscle atrophy.
    Summary · context
    AMPK/PGC-1α signal was detected by western blot and activated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR).
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In denervated mice with SESN2 knockdown, exogenous AMPK/PGC-1α activation with AICAR led to muscle mass retention.

    In plain wordsIn denervated mice with SESN2 knockdown, AICAR pathway activation preserved muscle mass compared with knockdown alone.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMuscle mass retention
    Study

    mousen: not reported in source

    Denervated muscle with SESN2 knockdown
    Comparator
    SESN2 knockdown without exogenous pathway activation
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous activation of AMPK/PGC-1α signaling could counteract the addition of slow-to-fast myofiber shift caused by SESN2 knockdown and lead to the retainment of muscle mass after denervation.
    2 context sentences
    Summary · context
    A mouse sciatic nerve transection model was created to evaluate denervated muscle atrophy.
    Summary · context
    AMPK/PGC-1α signal was detected by western blot and activated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR).

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

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