The mitochondrial-derived peptide MOTS-c suppresses ferroptosis and alleviates acute lung injury induced by myocardial ischemia reperfusion via PPARγ signaling pathway.

Lu P, Li X, Li B, Li X, Wang C, Liu Z, Ji Y, Wang X, Wen Z, Fan J, Yi C, Song M, Wang X

European journal of pharmacology7 Jun 2023Cited by 25 (Europe PMC)

PMID37290680DOI10.1016/j.ejphar.2023.175835PepBankPUB-37290680

Publisher page PubMedAsk about this study

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 study5

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

01AnimalAnimal study (in vivo)Efficacy outcome
In rats with myocardial ischemia reperfusion injury, MOTS‑c suppressed lung ferroptosis.
In plain wordsIn rats with lung injury after a heart blood-flow insult, MOTS‑c reduced a form of cell death called ferroptosis.
Peptide
MOTS-c
Outcome
DecreaseFerroptosis in MIR-induced ALI
Study
ratn: not reported in source
Sprague-Dawley rats with myocardial ischemia reperfusion-induced ALI
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
MOTS-c suppressed ferroptosis and alleviated ALI induced by MIR
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, we pretreated Sprague-Dawley rats with MOTS-c, Ferrostatin-1 and Fe-citrate(Ⅲ).
Report a problemFND-3729068002
02AnimalAnimal study (in vivo)Efficacy outcome
In rats with myocardial ischemia reperfusion injury, MOTS‑c alleviated acute lung injury.
In plain wordsIn rats with lung injury after a heart blood-flow insult, MOTS‑c eased the lung injury.
Peptide
MOTS-c
Outcome
DecreaseAcute lung injury after MIR
Study
ratn: not reported in source
Sprague-Dawley rats with myocardial ischemia reperfusion-induced ALI
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
MOTS-c suppressed ferroptosis and alleviated ALI induced by MIR
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, we pretreated Sprague-Dawley rats with MOTS-c, Ferrostatin-1 and Fe-citrate(Ⅲ).
Report a problemFND-3729068003
03AnimalAnimal study (in vivo)Mechanism
In rats with myocardial ischemia reperfusion injury, the protective effect of MOTS‑c depended on the PPARγ signaling pathway.
In plain wordsIn rats, the lung protection from MOTS‑c worked through the PPARγ pathway.
Peptide
MOTS-c
Outcome
Not applicablePPARγ dependence of MOTS-c protection
Study
ratn: not reported in source
Sprague-Dawley rats with myocardial ischemia reperfusion-induced ALI
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
and the protective effect of MOTS-c- was dependent on PPARγ signaling pathway
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, we pretreated Sprague-Dawley rats with MOTS-c, Ferrostatin-1 and Fe-citrate(Ⅲ).
Report a problemFND-3729068004
04LabIn vitro (cells)Mechanism
In mouse lung epithelial MLE-12 cells, MOTS‑c inhibited hypoxia regeneration-induced ferroptosis through the PPARγ signaling pathway.
In plain wordsIn mouse lung cells in the lab, MOTS‑c reduced a form of cell death called ferroptosis, through the PPARγ pathway.
Peptide
MOTS-c
Outcome
DecreaseFerroptosis in MLE-12 cells under hypoxia regeneration
Study
mousen: not reported in source
MLE-12 lung epithelial cells under hypoxia regeneration
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
MOTS-c inhibited ferroptosis against HR through the PPARγ signaling pathway.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, we evaluated the effect of MOTS-c on hypoxia regeneration (HR)-induced mouse lung epithelial-12 (MLE-12) ferroptosis and analyzed the expression of PPARγ through western blotting.
Report a problemFND-3729068005

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.

05HumanEndogenous levelObservational studyOther
In patients undergoing off-pump CABG, circulating MOTS‑c levels were lower in those with postoperative acute lung injury.
In plain wordsIn heart surgery patients, the body's own MOTS‑c in blood was lower in those who developed acute lung injury.
Peptide
MOTS-c
Outcome
DecreaseCirculating MOTS-c after off-pump CABG with ALI
Study
n: not reported in source
Comparator
Patients without postoperative ALI
Outcome group
Inflammation markers · Respiratory
Source sentences
Summary
circulating MOTS-c levels were decreased in postoperative ALI patients after off-pump CABG
1 context sentence(design, population, supporting numbers)
Summary · context
In humans, we used ELISA kits to investigate MOTS-c and malondialdehyde (MDA) levels in patients undergoing off-pump coronary artery bypass grafting (CABG).
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3729068001

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.

Version 2Current
10 Oct 2026, 08:19 UTC
Study results updated
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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