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Study · Not a test of the peptide alone · 2023

3 results

Exercise maintains bone homeostasis by promoting osteogenesis through STAT3.

Huang X, Zhu Y, Sun S, Gao X, Yang Y, Xu H, Jin A, Liu Y, Jia H, Dai Q, Jiang L

International journal of biological sciences2 Apr 2023Cited by 24 (Europe PMC)

PMID37151888 (opens in a new tab)PMCIDPMC10158023 (opens in a new tab)DOI10.7150/ijbs.82744 (opens in a new tab)PepBankPUB-37151888
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Summary

Bone exhibits changes in density, strength, and microarchitecture in relation to mechanical loading mediated by exercise. Appropriate exercise maintains bone homeostasis, while the absence of exercise leads to disuse bone loss. However, the acting mechanism of mechanotransduction in bone remains unclear. We performed the running-wheel exercise and tail suspension model to study the effects of exercise on bone metabolism, and found that osteoblastic Signal transducer and activator of transcription 3 (STAT3) activity was closely related to exercise-induced bone mass and metabolism changes. With the Flexcell tension-loading system in vitro, mechanical force promoted STAT3 activity, which was accompanied by increased osteoblastic differentiation of the bone marrow mesenchymal stem cells (BMSCs). In contrast, the inhibition of STAT3 phosphorylation blocked force-induced osteoblastic differentiation. Furthermore, pharmacological inactivation of STAT3 impaired the increase in exercise-induced bone mass and osteogenesis. With an inducible conditional deletion mouse model, we found that the osteoblast lineage-specific Stat3 deletion could also block force-induced osteoblastic differentiation in vitro and impair exercise-promoted bone mass and osteogenesis in vivo. This confirmed the crucial role of osteoblastic STAT3 in exercise-mediated bone metabolism. Finally, colivelin, a STAT3 agonist, promoted osteoblastic differentiation in vitro and partly rescued exercise loss-induced disuse bone loss by improving osteogenesis in the tail suspension model. Taken together, our study revealed the essential role of STAT3 in maintaining exercise-mediated bone homeostasis. In addition, STAT3 might act as a potential target for osteoporosis caused by exercise loss.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone3

In this study, Colivelin was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Colivelin.

  1. 01AnimalNot a test of Colivelin aloneAnimal study (in vivo)Efficacy outcome

    In the tail suspension model, colivelin partly reduced exercise loss-induced disuse bone loss.

    In plain wordsIn animals in the tail suspension model, colivelin partly reduced bone loss caused by exercise loss.

    Peptide
    Colivelin
    Outcome
    DecreaseDisuse bone loss
    Study

    n: not reported in source

    tail suspension model
    Outcome group
    Bone and joint · Musculoskeletal

    Source sentences

    Summary
    Finally, colivelin, a STAT3 agonist, promoted osteoblastic differentiation in vitro and partly rescued exercise loss-induced disuse bone loss by improving osteogenesis in the tail suspension model.

    In this study, Colivelin was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Colivelin.

  2. 02AnimalNot a test of Colivelin aloneAnimal study (in vivo)Efficacy outcome

    In the tail suspension model, colivelin improved osteogenesis.

    In plain wordsIn animals in the tail suspension model, colivelin improved bone formation.

    Peptide
    Colivelin
    Outcome
    IncreaseOsteogenesis
    Study

    n: not reported in source

    tail suspension model
    Outcome group
    Bone and joint · Musculoskeletal

    Source sentences

    Summary
    Finally, colivelin, a STAT3 agonist, promoted osteoblastic differentiation in vitro and partly rescued exercise loss-induced disuse bone loss by improving osteogenesis in the tail suspension model.

    In this study, Colivelin was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Colivelin.

  3. 03LabNot a test of Colivelin aloneIn vitro (cells)Efficacy outcome

    In vitro, colivelin promoted osteoblastic differentiation.

    In plain wordsIn lab tests, colivelin promoted the development of bone-forming cells.

    Peptide
    Colivelin
    Outcome
    IncreaseOsteoblastic differentiation
    Study

    n: not reported in source

    osteoblastic differentiation in vitro
    Outcome group
    Bone and joint · Musculoskeletal

    Source sentences

    Summary
    Finally, colivelin, a STAT3 agonist, promoted osteoblastic differentiation in vitro

    In this study, Colivelin was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Colivelin.

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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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