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Study · In vitro (cells) · mouse · 2025

8 results

Kisspeptin-54 ameliorates chondrocyte senescence in osteoarthritis via SIRT3-mediated telomere protection and p53 acetylation inhibition.

Yang Z, Li J, Jin W, Cai D, Zhang J, Hong S

Neuropeptides19 Sept 2025Cited by 2 (Europe PMC)

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 study8

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 at up to 200 nM rescued cell viability.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 at up to 200 nM rescued cell survival.

    Outcome
    IncreaseCell viability under TBHP
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    <=200 nMAs given in this study (mouse).

    Source sentences

    Summary
    Kisspeptin-54 (≤200 nM) rescued cell viability
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  2. 02LabIn vitro (cells)Efficacy outcome

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 reduced LDH release by 57 % at 200 nM.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 lowered cell damage release by 57 % at 200 nM.

    Outcome
    DecreaseLDH release
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    200 nMAs given in this study (mouse).

    Measurements

    LDH release reduction
    57%
    200 nM

    Source sentences

    Summary
    Kisspeptin-54 (≤200 nM) rescued cell viability, reduced LDH release (57 % at 200 nM)
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  3. 03LabIn vitro (cells)Efficacy outcome

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 mitigated the rise in reactive oxygen species.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 reduced reactive oxygen species.

    Outcome
    DecreaseROS level
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    10-1000 nMAs given in this study (mouse).

    Source sentences

    Summary
    Kisspeptin-54 (≤200 nM) rescued cell viability, reduced LDH release (57 % at 200 nM), and mitigated ROS and SOD activity decline
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  4. 04LabIn vitro (cells)Efficacy outcome

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 mitigated the decline in SOD activity.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 limited the loss of antioxidant SOD activity.

    Outcome
    IncreaseSOD activity decline
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    10-1000 nMAs given in this study (mouse).

    Source sentences

    Summary
    Kisspeptin-54 (≤200 nM) rescued cell viability, reduced LDH release (57 % at 200 nM), and mitigated ROS and SOD activity decline
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  5. 05LabIn vitro (cells)Mechanism

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 restored SIRT3 expression.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 restored the protein SIRT3.

    Outcome
    IncreaseSIRT3 expression
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    10-1000 nMAs given in this study (mouse).

    Source sentences

    Summary
    Kisspeptin-54 restored SIRT3 expression
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  6. 06LabIn vitro (cells)Mechanism

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 suppressed p53 acetylation, with Acetyl-p53[K382] reduced by 56 % at 200 nM.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 lowered a p53 change linked to aging by 56 % at 200 nM.

    Outcome
    Decreasep53 acetylation
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    200 nMAs given in this study (mouse).

    Measurements

    Acetyl-p53[K382] reduction
    56%
    200 nM

    Source sentences

    Summary
    suppressed p53 acetylation (Acetyl-p53[K382] reduced by 56 % at 200 nM)
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.
  7. 07LabIn vitro (cells)Mechanism

    In primary mouse chondrocytes treated with TBHP, Kisspeptin‑54 preserved telomere function, with telomere length restored to 91 % of control.

    In plain wordsIn mouse cartilage cells under oxidative stress, Kisspeptin‑54 restored telomere length to 91 % of control.

    Outcome
    IncreaseTelomere length
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    10-1000 nMAs given in this study (mouse).

    Measurements

    Telomere length restored
    91 % of control
    Kisspeptin-54

    Source sentences

    Summary
    preserved telomere function (telomere length restored to 91 % of control)
    1 context sentence
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.

Studies that did not test the peptide alone1

In this study, Kisspeptin-54 (metastin) 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 Kisspeptin-54 (metastin).

  1. 08LabNot a test of Kisspeptin-54 (metastin) aloneIn vitro (cells)Mechanism

    In primary mouse chondrocytes, SIRT3 knockdown abrogated the effects of Kisspeptin‑54.

    In plain wordsIn mouse cartilage cells, switching off SIRT3 removed the effects of Kisspeptin‑54.

    Outcome
    DecreaseKisspeptin-54 effects after SIRT3 knockdown
    Study

    mousen: not reported in source

    primary mouse chondrocytes treated with TBHP
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    SIRT3 knockdown abrogated these effects, confirming its critical role.
    2 context sentences
    Summary · context
    Kisspeptin-54 was administered at varying concentrations (10-1000 nM) to assess cytoprotection, while SIRT3 was knocked down using adenoviral shRNA to validate mechanistic pathways.
    Summary · context
    Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP.

    In this study, Kisspeptin-54 (metastin) 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 Kisspeptin-54 (metastin).

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

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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