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Study · In vitro (cells) · 2025

7 results

Kisspeptin-10 Protects Against TNF-α-Induced Chondrocyte Senescence via the SIRT1/p53/p21 Signaling.

Qiu J, Chen G, Peng G, Qu G, Ren T, Deng J

Journal of biochemical and molecular toxicology1 Jun 2025Cited by 1 (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 study7

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In chondrocytes with TNF-α-induced senescence, kisspeptin‑10 at 50 and 100 nM reduced senescence-associated β-galactosidase staining.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 reduced a stain that marks ageing cells.

    Outcome
    DecreaseSenescence-associated β-galactosidase staining
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    50 and 100 nMAs given in this study.

    Source sentences

    Summary
    Kp-10 treatment at concentrations of 50 and 100 nM effectively ameliorated TNF-α-induced senescence, as evidenced by diminished senescence-associated β-galactosidase staining and enhanced telomerase activity.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.
  2. 02LabIn vitro (cells)Efficacy outcome

    In chondrocytes with TNF-α-induced senescence, kisspeptin‑10 at 50 and 100 nM enhanced telomerase activity.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 raised telomerase activity, which is linked to cell ageing.

    Outcome
    IncreaseTelomerase activity
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    50 and 100 nMAs given in this study.

    Source sentences

    Summary
    Kp-10 treatment at concentrations of 50 and 100 nM effectively ameliorated TNF-α-induced senescence, as evidenced by diminished senescence-associated β-galactosidase staining and enhanced telomerase activity.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.
  3. 03LabIn vitro (cells)Mechanism

    In chondrocytes with TNF-α-induced senescence, kisspeptin‑10 modulated the expression of the cell-ageing regulators hTERT and TERF2.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 changed the activity of two genes that regulate cell ageing.

    Outcome
    Direction not reportedhTERT and TERF2 expression
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Kisspeptin-10 modulated the expression of key regulators involved in cellular aging, including hTERT and TERF2, and suppressed the activation of the p53/p21 pathway.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.
  4. 04LabIn vitro (cells)Mechanism

    In chondrocytes with TNF-α-induced senescence, kisspeptin‑10 suppressed activation of the p53/p21 pathway.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 switched off a pathway that drives cell ageing.

    Outcome
    Decreasep53/p21 pathway activation
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    suppressed the activation of the p53/p21 pathway.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.
  5. 05LabIn vitro (cells)Mechanism

    In chondrocytes, kisspeptin‑10 restored SIRT1 expression that TNF-α had reduced.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 restored SIRT1, a protein that TNF-α had lowered.

    Outcome
    IncreaseSIRT1 expression
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, Kp-10 restored SIRT1 expression, which was downregulated by TNF-α.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.
  6. 06LabIn vitro (cells)Mechanism

    Silencing SIRT1 abolished the protective effects of kisspeptin‑10 in chondrocytes, which shows that SIRT1 is needed for its anti-senescence action.

    In plain wordsIn cartilage cells in the lab, kisspeptin‑10 lost its protective effect when SIRT1 was silenced.

    Outcome
    Not applicableSIRT1 silencing and the effect of Kp-10
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Silencing SIRT1 abolished the protective effects of Kp-10, highlighting the essential role of SIRT1 in its anti-senescence action.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.

Studies that did not test the peptide alone1

In this study, Kisspeptin-10 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-10.

  1. 07LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In chondrocytes, TNF-α treatment dose-dependently decreased expression of the kisspeptin‑10 receptor Gpr54.

    In plain wordsIn cartilage cells in the lab, TNF-α lowered the receptor for kisspeptin‑10 in a dose-dependent way.

    Outcome
    Not applicableGpr54 expression after TNF-α
    Study

    n: not reported in source

    Primary chondrocytes and ATDC5 chondrogenic cells with TNF-α-induced senescence
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Gpr54 expression was confirmed in both primary chondrocytes and the ATDC5 chondrogenic cell line, with TNF-α treatment leading to a dose-dependent decrease in Gpr54 expression.
    1 context sentence
    Summary · context
    This study investigates the role of Kp-10 in mitigating TNF-α- induced senescence in primary chondrocytes, a hallmark of OA pathogenesis.

    In this study, Kisspeptin-10 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-10.

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, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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