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Study · Animal study (in vivo) · mouse · 2026

10 results

Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.

Xing L, Lu B, Zhu X, Al Saeedi M, Lerman A, Eirin A, Cohen P, Lerman LO

Inflammation and regeneration22 Jun 2026

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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study10

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with renal artery stenosis, MOTS‑c-pretreated MSCs did not improve renal perfusion.

    In plain wordsIn mice with narrowed kidney arteries, cells pretreated with MOTS‑c did not improve blood flow to the kidney.

    Peptide
    MOTS-c
    Outcome
    No significant changeRenal perfusion with MOTS-c-pretreated obese MSCs
    Study

    mousen: not reported in source

    Renal artery stenosis
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, in a murine model of renal artery stenosis, MOTS-c-pretreated MSCs failed to improve renal perfusion, fibrosis, or tubular injury
    1 context sentence
    Summary · context
    In vivo, the effects of MOTS-c pre-treatment on the reparative capacity of obese MSC were tested in stenotic mouse kidneys.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with renal artery stenosis, MOTS‑c-pretreated MSCs did not improve renal fibrosis.

    In plain wordsIn mice with narrowed kidney arteries, cells pretreated with MOTS‑c did not reduce kidney scarring.

    Peptide
    MOTS-c
    Outcome
    No significant changeRenal fibrosis with MOTS-c-pretreated obese MSCs
    Study

    mousen: not reported in source

    Renal artery stenosis
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, in a murine model of renal artery stenosis, MOTS-c-pretreated MSCs failed to improve renal perfusion, fibrosis, or tubular injury
    1 context sentence
    Summary · context
    In vivo, the effects of MOTS-c pre-treatment on the reparative capacity of obese MSC were tested in stenotic mouse kidneys.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with renal artery stenosis, MOTS‑c-pretreated MSCs did not improve tubular injury.

    In plain wordsIn mice with narrowed kidney arteries, cells pretreated with MOTS‑c did not reduce kidney tubule damage.

    Peptide
    MOTS-c
    Outcome
    No significant changeTubular injury with MOTS-c-pretreated obese MSCs
    Study

    mousen: not reported in source

    Renal artery stenosis
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, in a murine model of renal artery stenosis, MOTS-c-pretreated MSCs failed to improve renal perfusion, fibrosis, or tubular injury
    1 context sentence
    Summary · context
    In vivo, the effects of MOTS-c pre-treatment on the reparative capacity of obese MSC were tested in stenotic mouse kidneys.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with renal artery stenosis, MOTS‑c pretreatment blunted the reparative efficacy of lean MSCs.

    In plain wordsIn mice with narrowed kidney arteries, MOTS‑c pretreatment made cells from lean donors less able to repair the kidney.

    Peptide
    MOTS-c
    Outcome
    DecreaseReparative efficacy of lean MSCs after MOTS-c pretreatment
    Study

    mousen: not reported in source

    Renal artery stenosis
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    while pretreatment also blunted the reparative efficacy of lean MSCs.
    1 context sentence
    Summary · context
    In vivo, the effects of MOTS-c pre-treatment on the reparative capacity of obese MSC were tested in stenotic mouse kidneys.
  5. 05LabIn vitro (cells)Mechanism

    Exogenous MOTS‑c restored intracellular MOTS‑c levels in MSCs from donors with obesity.

    In plain wordsIn lab cells from donors with obesity, added MOTS‑c brought the cells' MOTS‑c levels back up.

    Peptide
    MOTS-c
    Outcome
    IncreaseIntracellular MOTS-c level
    Study

    humann: not reported in source

    Obese adipose-derived MSCs
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    exogenous MOTS-c restored intracellular levels
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group) were assessed in vitro for changes in proliferation, senescence (p16, p21) TNF-α, and antioxidant gene expression following MOTS-c co-incubation.
  6. 06LabIn vitro (cells)Mechanism

    Exogenous MOTS‑c activated AMPK signaling in MSCs from donors with obesity.

    In plain wordsIn lab cells from donors with obesity, MOTS‑c switched on the AMPK energy-sensing pathway.

    Peptide
    MOTS-c
    Outcome
    IncreaseAMPK signaling
    Study

    humann: not reported in source

    Obese adipose-derived MSCs
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    activated AMPK signaling in obese MSCs
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group) were assessed in vitro for changes in proliferation, senescence (p16, p21) TNF-α, and antioxidant gene expression following MOTS-c co-incubation.
  7. 07LabIn vitro (cells)Efficacy outcome

    Exogenous MOTS‑c reduced proliferation of MSCs from donors with obesity.

    In plain wordsIn lab cells from donors with obesity, MOTS‑c slowed cell growth.

    Peptide
    MOTS-c
    Outcome
    DecreaseMSC proliferation
    Study

    humann: not reported in source

    Obese adipose-derived MSCs
    Outcome group
    Aging markers · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    it reduced proliferation, increased expression of senescence-associated genes (p16, p21), and upregulated TNF-α
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group) were assessed in vitro for changes in proliferation, senescence (p16, p21) TNF-α, and antioxidant gene expression following MOTS-c co-incubation.
  8. 08LabIn vitro (cells)Efficacy outcome

    Exogenous MOTS‑c increased expression of the senescence-associated genes p16 and p21 in MSCs from donors with obesity.

    In plain wordsIn lab cells from donors with obesity, MOTS‑c raised signs of cell ageing (p16 and p21).

    Peptide
    MOTS-c
    Outcome
    IncreaseSenescence-associated genes (p16, p21)
    Study

    humann: not reported in source

    Obese adipose-derived MSCs
    Outcome group
    Aging markers · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    increased expression of senescence-associated genes (p16, p21)
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group) were assessed in vitro for changes in proliferation, senescence (p16, p21) TNF-α, and antioxidant gene expression following MOTS-c co-incubation.
  9. 09LabIn vitro (cells)Efficacy outcome

    Exogenous MOTS‑c upregulated TNF-α in MSCs from donors with obesity.

    In plain wordsIn lab cells from donors with obesity, MOTS‑c raised the inflammation signal TNF-α.

    Peptide
    MOTS-c
    Outcome
    IncreaseTNF-α expression
    Study

    humann: not reported in source

    Obese adipose-derived MSCs
    Outcome group
    Inflammation markers · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and upregulated TNF-α.
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group) were assessed in vitro for changes in proliferation, senescence (p16, p21) TNF-α, and antioxidant gene expression following MOTS-c co-incubation.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 10LabEndogenous levelIn vitro (cells)Other

    Basal MOTS‑c expression was lower in MSCs from donors with obesity than in MSCs from lean donors.

    In plain wordsCells from donors with obesity made less of the body's own MOTS‑c than cells from lean donors.

    Peptide
    MOTS-c
    Outcome
    DecreaseBasal MOTS-c expression in obese vs lean MSCs
    Study

    humann = 12

    Adipose-derived MSCs
    Comparator
    Lean MSCs
    Outcome group
    Mitochondrial function · Metabolic and weight

    Source sentences

    Summary
    Basal MOTS-c expression was lower in obese vs. lean MSCs.
    1 context sentence
    Summary · context
    MSCs isolated from abdominal fat of patients with obesity (BMI ≥ 30 kg/m2) and lean donors (BMI 2) (n = 6/group)

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

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, 08:19 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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