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Study · Animal study (in vivo) · 2025

10 results

MOTS-c Promotes Glycolysis via AMPK-HIF-1α-PFKFB3 Pathway to Ameliorate Cardiopulmonary Bypass-induced Lung Injury.

Shen Z, Lu P, Jin W, Wen Z, Qi Y, Li X, Chu M, Yao X, Wu M, Wang A, Zhang X, Wang W, Song M, Wang X

American journal of respiratory cell and molecular biology1 Sept 2025Cited by 14 (Europe PMC)

PMID40035775 (opens in a new tab)DOI10.1165/rcmb.2024-0533oc (opens in a new tab)PepBankPUB-40035775
Publisher pagePubMedAsk about this study
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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 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 vivo, MOTS‑c pretreatment alleviated lung ischemia-reperfusion injury.

    In plain wordsIn animals, MOTS‑c given beforehand reduced lung injury caused by blocked and restored blood flow.

    Peptide
    MOTS-c
    Outcome
    DecreaseLung ischemia-reperfusion injury
    Study

    n: not reported in source

    Outcome group
    Cardiovascular events · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo and in vitro experiments demonstrated that MOTS-c pretreatment alleviated LIRI by enhancing glycolytic flux, reducing oxidative stress, and suppressing ferroptosis in pulmonary microvascular endothelial cells.
  2. 02LabIn vitro (cells)Mechanism

    In pulmonary microvascular endothelial cells, MOTS‑c pretreatment enhanced glycolytic flux.

    In plain wordsIn lab cells, MOTS‑c given beforehand increased the cells' sugar-burning activity.

    Peptide
    MOTS-c
    Outcome
    IncreaseGlycolytic flux
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo and in vitro experiments demonstrated that MOTS-c pretreatment alleviated LIRI by enhancing glycolytic flux, reducing oxidative stress, and suppressing ferroptosis in pulmonary microvascular endothelial cells.
  3. 03LabIn vitro (cells)Mechanism

    In pulmonary microvascular endothelial cells, MOTS‑c pretreatment reduced oxidative stress.

    In plain wordsIn lab cells, MOTS‑c given beforehand lowered oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo and in vitro experiments demonstrated that MOTS-c pretreatment alleviated LIRI by enhancing glycolytic flux, reducing oxidative stress, and suppressing ferroptosis in pulmonary microvascular endothelial cells.
  4. 04LabIn vitro (cells)Mechanism

    In pulmonary microvascular endothelial cells, MOTS‑c pretreatment suppressed ferroptosis.

    In plain wordsIn lab cells, MOTS‑c given beforehand reduced a type of iron-dependent cell death.

    Peptide
    MOTS-c
    Outcome
    DecreaseFerroptosis
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo and in vitro experiments demonstrated that MOTS-c pretreatment alleviated LIRI by enhancing glycolytic flux, reducing oxidative stress, and suppressing ferroptosis in pulmonary microvascular endothelial cells.
  5. 05LabIn vitro (cells)Mechanism

    MOTS‑c reinstated expression of the glycolytic enzyme PFKFB3.

    In plain wordsIn lab tests, MOTS‑c restored levels of a sugar-burning enzyme called PFKFB3.

    Peptide
    MOTS-c
    Outcome
    IncreasePFKFB3 expression
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In particular, MOTS-c reinstated the expression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), an essential glycolytic enzyme, thus preserving cellular energy homeostasis and diminishing lipid peroxidation.
  6. 06LabIn vitro (cells)Mechanism

    MOTS‑c diminished lipid peroxidation, linked to restored PFKFB3 expression.

    In plain wordsIn lab tests, MOTS‑c reduced fat damage caused by oxidation.

    Peptide
    MOTS-c
    Outcome
    DecreaseLipid peroxidation
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In particular, MOTS-c reinstated the expression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), an essential glycolytic enzyme, thus preserving cellular energy homeostasis and diminishing lipid peroxidation.
  7. 07LabIn vitro (cells)Mechanism

    MOTS‑c elevated phosphorylated AMPKα.

    In plain wordsIn lab tests, MOTS‑c raised the active form of an energy-sensing protein.

    Peptide
    MOTS-c
    Outcome
    IncreasePhosphorylated AMPKα expression
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c elevated phosphorylated AMPKα and HIF-1α expression, indicating a vital function for these pathways in enhancing glycolysis and antioxidant defenses.
  8. 08LabIn vitro (cells)Mechanism

    MOTS‑c elevated HIF-1α expression.

    In plain wordsIn lab tests, MOTS‑c raised levels of the protein HIF-1α.

    Peptide
    MOTS-c
    Outcome
    IncreaseHIF-1α expression
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c elevated phosphorylated AMPKα and HIF-1α expression, indicating a vital function for these pathways in enhancing glycolysis and antioxidant defenses.
  9. 09LabIn vitro (cells)Mechanism

    Genetic and pharmacological inhibition of PFKFB3 abrogated the protective effects of MOTS‑c.

    In plain wordsIn lab tests, blocking the enzyme PFKFB3 removed the protective effects of MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    Not applicableDependence of MOTS-c protection on PFKFB3
    Study

    n: not reported in source

    pulmonary microvascular endothelial cells
    Comparator
    PFKFB3 inhibition
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Genetic and pharmacological inhibition of PFKFB3 abrogated the protective effects of MOTS-c, thereby confirming the essential role of PFKFB3-mediated glycolysis in alleviating LIRI.

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. 10HumanEndogenous levelObservational studyOther

    In patients undergoing cardiopulmonary bypass, plasma MOTS‑c concentrations were significantly lower in those with acute lung injury.

    In plain wordsIn patients having heart bypass surgery, the body's own MOTS‑c levels were lower in those who developed lung injury.

    Peptide
    MOTS-c
    Outcome
    DecreasePlasma MOTS-c in patients with acute lung injury after CPB
    Study

    n = 107

    Outcome group
    Inflammation markers · Respiratory

    Source sentences

    Summary
    MOTS-c concentrations were significantly reduced in patients with ALI.
    1 context sentence
    Summary · context
    We conducted a prospective, controlled trial involving 107 patients undergoing CPB, evaluating plasma concentrations of MOTS-c and inflammatory markers.

    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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