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

7 results

MOTS-c inhibits Osteolysis in the Mouse Calvaria by affecting osteocyte-osteoclast crosstalk and inhibiting inflammation.

Yan Z, Zhu S, Wang H, Wang L, Du T, Ye Z, Zhai D, Zhu Z, Tian X, Lu Z, Cao X

Pharmacological research29 Jul 2019Cited by 57 (Europe PMC)

PMID31369811 (opens in a new tab)DOI10.1016/j.phrs.2019.104381 (opens in a new tab)PepBankPUB-31369811
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: 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)Efficacy outcome

    In a mouse model of UHMWPE particle-induced osteolysis, MOTS‑c treatment alleviated bone erosion.

    In plain wordsIn mice with particle-induced bone loss, MOTS‑c treatment reduced bone erosion.

    Peptide
    MOTS-c
    Outcome
    DecreaseBone erosion
    Study

    mousen: not reported in source

    UHMWPE particle-induced osteolysis
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we demonstrate that MOTS-c treatment in ultra-high molecular weight polyethylene (UHMWPE) particle-induced osteolysis mouse model alleviated bone erosion and inflammation.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a mouse model of UHMWPE particle-induced osteolysis, MOTS‑c treatment alleviated inflammation.

    In plain wordsIn mice with particle-induced bone loss, MOTS‑c treatment reduced inflammation.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammation
    Study

    mousen: not reported in source

    UHMWPE particle-induced osteolysis
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we demonstrate that MOTS-c treatment in ultra-high molecular weight polyethylene (UHMWPE) particle-induced osteolysis mouse model alleviated bone erosion and inflammation.
  3. 03LabIn vitro (cells)Mechanism

    In osteocytes, MOTS‑c increased the osteoprotegerin to RANKL ratio.

    In plain wordsIn cells, MOTS‑c raised the ratio of OPG to RANKL in bone cells called osteocytes.

    Peptide
    MOTS-c
    Outcome
    IncreaseOPG/RANKL ratio in osteocytes
    Study

    n: not reported in source

    Osteocytes
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c increased osteoprotegerin (OPG)/ receptor activator of nuclear factor kappa-B ligand (RANKL) ratio in osteocytes, leading to inhibition of osteoclastogenesis.
  4. 04LabIn vitro (cells)Mechanism

    In osteocyte experiments, the MOTS‑c-induced rise in OPG/RANKL ratio led to inhibition of osteoclastogenesis.

    In plain wordsIn cells, MOTS‑c reduced the formation of bone-resorbing osteoclasts.

    Peptide
    MOTS-c
    Outcome
    DecreaseOsteoclastogenesis
    Study

    n: not reported in source

    Osteocytes
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c increased osteoprotegerin (OPG)/ receptor activator of nuclear factor kappa-B ligand (RANKL) ratio in osteocytes, leading to inhibition of osteoclastogenesis.
  5. 05LabIn vitro (cells)Mechanism

    In primary bone marrow macrophages, MOTS‑c alleviated the STAT1 phosphorylation triggered by UHMWPE particles.

    In plain wordsIn cells, MOTS‑c reduced the STAT1 signal triggered by plastic particles.

    Peptide
    MOTS-c
    Outcome
    DecreaseSTAT1 phosphorylation
    Study

    n: not reported in source

    Primary bone marrow macrophages
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In primary bone marrow macrophages (BMMs) MOTS-c alleviated STAT1 and NF-κB phosphorylation triggered by UHMWPE particles.
  6. 06LabIn vitro (cells)Mechanism

    In primary bone marrow macrophages, MOTS‑c alleviated the NF-κB phosphorylation triggered by UHMWPE particles.

    In plain wordsIn cells, MOTS‑c reduced the NF-κB signal triggered by plastic particles.

    Peptide
    MOTS-c
    Outcome
    DecreaseNF-κB phosphorylation
    Study

    n: not reported in source

    Primary bone marrow macrophages
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In primary bone marrow macrophages (BMMs) MOTS-c alleviated STAT1 and NF-κB phosphorylation triggered by UHMWPE particles.
  7. 07LabIn vitro (cells)Mechanism

    Promoting ROS production or suppressing PGC-1α through AMPK repression blocked the anti-inflammatory effects of MOTS‑c.

    In plain wordsIn cells, the anti-inflammatory effects of MOTS‑c were blocked when ROS rose or when the AMPK-PGC-1α pathway was suppressed.

    Peptide
    MOTS-c
    Outcome
    Not applicableAnti-inflammatory effect of MOTS-c after ROS promotion or AMPK-PGC-1α repression
    Study

    n: not reported in source

    Bone marrow macrophages
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Promoting ROS production or suppressing peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) by adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) repression blocked these anti-inflammatory effects of MOTS-c treatment.

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

    9 Oct 2026, 18:17 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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