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Study · Animal study (in vivo) · rat · 2021

6 results

Kisspeptin preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain hippocampus and human neuronal cell line.

Mattam U, Talari NK, Paripati AK, Krishnamoorthy T, Sepuri NBV

Biochimica et biophysica acta. Molecular cell research11 Sept 2020Cited by 11 (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 study6

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In aging rats, in vivo Kp administration increased the number of mitochondria in the hippocampus.

    In plain wordsIn aging rats, kisspeptin‑10 increased the number of mitochondria in the brain.

    Outcome
    IncreaseMitochondrial number
    Study

    ratn: not reported in source

    Aging Wistar rat hippocampus
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Intriguingly, Kp administration in vivo also results in the enhancement of mitochondrial number, complex I activity, and Adenosine Triphosphate (ATP) levels.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In aging rats, in vivo Kp administration increased mitochondrial complex I activity.

    In plain wordsIn aging rats, kisspeptin‑10 increased the activity of a key mitochondrial enzyme complex.

    Outcome
    IncreaseMitochondrial complex I activity
    Study

    ratn: not reported in source

    Aging Wistar rat hippocampus
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Intriguingly, Kp administration in vivo also results in the enhancement of mitochondrial number, complex I activity, and Adenosine Triphosphate (ATP) levels.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In aging rats, in vivo Kp administration increased ATP levels.

    In plain wordsIn aging rats, kisspeptin‑10 increased levels of ATP, the cell's energy molecule.

    Outcome
    IncreaseATP levels
    Study

    ratn: not reported in source

    Aging Wistar rat hippocampus
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Intriguingly, Kp administration in vivo also results in the enhancement of mitochondrial number, complex I activity, and Adenosine Triphosphate (ATP) levels.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In aging Wistar rats, Kisspeptin‑10 induced autophagy and mitophagy in the hippocampus.

    In plain wordsIn aging rats, kisspeptin‑10 switched on the clean-up of damaged mitochondria in the brain.

    Outcome
    IncreaseAutophagy and mitophagy in aging rat hippocampus
    Study

    ratn: not reported in source

    Hippocampus of aging Wistar rats
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using SKNSH cell line, hippocampus explant cultures and hippocampus of aging Wistar rat models, we show that Kisspeptin-10 (Kp) induces autophagy and mitophagy
  5. 05LabIn vitro (cells)Mechanism

    In SKNSH cells and hippocampus explant cultures, Kisspeptin‑10 induced autophagy and mitophagy through a Ca2+/CaMKKbeta-AMPK-ULK1 pathway.

    In plain wordsIn lab-grown cells and brain tissue cultures, kisspeptin‑10 switched on the cell's clean-up of damaged mitochondria through a calcium-driven pathway.

    Outcome
    IncreaseAutophagy and mitophagy induction
    Study

    humann: not reported in source

    SKNSH cell line, hippocampus explant cultures
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we show that Kisspeptin-10 (Kp) induces autophagy and mitophagy via calcium, Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ), AMP-activated protein kinase (AMPK), and Unc-51 like autophagy activating kinase (ULK1) signaling pathway that is independent of mammalian target of rapamycin (mTOR).
  6. 06LabIn vitro (cells)Mechanism

    In SKNSH cells and hippocampus explant cultures, Kisspeptin‑10 induced autophagy through a pathway independent of mTOR.

    In plain wordsIn lab-grown cells and brain tissue cultures, kisspeptin‑10 started this clean-up process without using the mTOR pathway.

    Outcome
    No significant changemTOR dependence of Kp-induced autophagy
    Study

    humann: not reported in source

    SKNSH cell line, hippocampus explant cultures
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we show that Kisspeptin-10 (Kp) induces autophagy and mitophagy via calcium, Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ), AMP-activated protein kinase (AMPK), and Unc-51 like autophagy activating kinase (ULK1) signaling pathway that is independent of mammalian target of rapamycin (mTOR).

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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