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Study · Animal study (in vivo) · 2024

9 results

The mitochondrial genome-encoded peptide MOTS-c interacts with Bcl-2 to alleviate nonalcoholic steatohepatitis progression.

Lu H, Fan L, Zhang W, Chen G, Xiang A, Wang L, Lu Z, Zhai Y

Cell reports11 Jan 2024Cited by 19 (Europe PMC)

PMID38206815 (opens in a new tab)DOI10.1016/j.celrep.2023.113587 (opens in a new tab)PepBankPUB-38206815
Publisher pagePubMedAsk about this study
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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-ND. 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 a NASH-diet model, long-term preventive and short-term therapeutic MOTS‑c treatments alleviated liver steatosis.

    In plain wordsIn an animal model of fatty liver disease, MOTS‑c treatment reduced fat build-up in the liver.

    Peptide
    MOTS-c
    Outcome
    DecreaseLiver steatosis
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that long-term preventive and short-term therapeutic effects of MOTS-c treatments alleviate NASH-diet-induced liver steatosis, cellular apoptosis, inflammation, and fibrosis.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a NASH-diet model, MOTS‑c treatments alleviated cellular apoptosis.

    In plain wordsIn an animal model of fatty liver disease, MOTS‑c treatment reduced liver cell death.

    Peptide
    MOTS-c
    Outcome
    DecreaseCellular apoptosis
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that long-term preventive and short-term therapeutic effects of MOTS-c treatments alleviate NASH-diet-induced liver steatosis, cellular apoptosis, inflammation, and fibrosis.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In a NASH-diet model, MOTS‑c treatments alleviated inflammation.

    In plain wordsIn an animal model of fatty liver disease, MOTS‑c treatment reduced inflammation.

    Peptide
    MOTS-c
    Outcome
    DecreaseLiver inflammation
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that long-term preventive and short-term therapeutic effects of MOTS-c treatments alleviate NASH-diet-induced liver steatosis, cellular apoptosis, inflammation, and fibrosis.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In a NASH-diet model, MOTS‑c treatments alleviated fibrosis.

    In plain wordsIn an animal model of fatty liver disease, MOTS‑c treatment reduced liver scarring.

    Peptide
    MOTS-c
    Outcome
    DecreaseLiver fibrosis
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that long-term preventive and short-term therapeutic effects of MOTS-c treatments alleviate NASH-diet-induced liver steatosis, cellular apoptosis, inflammation, and fibrosis.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In a NASH-diet model, MOTS‑c significantly reversed NASH-induced mitochondrial metabolic deficiency.

    In plain wordsIn an animal model of fatty liver disease, MOTS‑c reversed a loss of mitochondrial function.

    Peptide
    MOTS-c
    Outcome
    IncreaseNASH-induced mitochondrial metabolic deficiency
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mitochondrial oxidative capacity and metabolites profiling analysis show that MOTS-c significantly reverses NASH-induced mitochondrial metabolic deficiency.
  6. 06AnimalAnimal study (in vivo)Mechanism

    MOTS‑c directly interacted with the BH3 domain of the antiapoptotic protein Bcl-2.

    In plain wordsIn lab and animal tests, MOTS‑c bound directly to the cell-survival protein Bcl-2.

    Peptide
    MOTS-c
    Outcome
    Not applicableBinding to the BH3 domain of Bcl-2
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, we identify that MOTS-c directly interacts with the BH3 domain of antiapoptotic B cell lymphoma-2 (Bcl-2), increases Bcl-2 protein stability, and suppresses Bcl-2 ubiquitination.
  7. 07AnimalAnimal study (in vivo)Mechanism

    MOTS‑c increased Bcl-2 protein stability.

    In plain wordsIn lab and animal tests, MOTS‑c made the Bcl-2 protein more stable.

    Peptide
    MOTS-c
    Outcome
    IncreaseBcl-2 protein stability
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, we identify that MOTS-c directly interacts with the BH3 domain of antiapoptotic B cell lymphoma-2 (Bcl-2), increases Bcl-2 protein stability, and suppresses Bcl-2 ubiquitination.
  8. 08AnimalAnimal study (in vivo)Mechanism

    MOTS‑c suppressed Bcl-2 ubiquitination.

    In plain wordsIn lab and animal tests, MOTS‑c reduced the tagging of Bcl-2 for breakdown.

    Peptide
    MOTS-c
    Outcome
    DecreaseBcl-2 ubiquitination
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, we identify that MOTS-c directly interacts with the BH3 domain of antiapoptotic B cell lymphoma-2 (Bcl-2), increases Bcl-2 protein stability, and suppresses Bcl-2 ubiquitination.
  9. 09AnimalAnimal study (in vivo)Mechanism

    With a Bcl-2 inhibitor or Bcl-2 knockdown, the improvement by MOTS‑c of NASH-induced mitochondrial dysfunction, inflammation and fibrosis depended on Bcl-2 function.

    In plain wordsIn NASH models, the benefits of MOTS‑c depended on the Bcl-2 protein.

    Peptide
    MOTS-c
    Outcome
    Not applicableBcl-2 dependence of MOTS-c benefit on mitochondrial dysfunction, inflammation and fibrosis
    Study

    n: not reported in source

    NASH-diet-induced steatohepatitis
    Comparator
    Bcl-2 inhibitor or AAV-mediated Bcl-2 knockdown
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    By using a Bcl-2 inhibitor or adeno-associated virus (AAV)-mediated Bcl-2 knockdown, we further confirm that MOTS-c improves NASH-induced mitochondrial dysfunction, inflammation, and fibrosis, which are dependent on Bcl-2 function.

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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