MOTS-c attenuates cardiac dysfunction following high altitude exposure by promoting mitophagy.

Feng Z, Xing Y, Lou J, Li H, Zhang Z, Li M, Zhu Q, Cui Y, Li J, Gao F, Yi W, Sun Y, Zhang X

Free radical biology & medicine5 Feb 2026Cited by 1 (Europe PMC)

PMID41654147DOI10.1016/j.freeradbiomed.2026.01.064PepBankPUB-41654147

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: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice, exogenous MOTS‑c supplementation during de-acclimatization alleviated cardiac dysfunction after high-altitude exposure.
In plain wordsIn mice, giving MOTS‑c after return from high altitude reduced heart problems caused by high altitude.
Peptide
MOTS-c
Outcome
DecreaseCardiac dysfunction after high-altitude exposure
Study
mousen: not reported in source
High-altitude exposure and de-acclimatization model
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated · During de-acclimatizationAs given in this study (mouse).
Source sentences
Summary
Exogenous supplementation of MOTS-c during de-acclimatization effectively alleviated the cardiac dysfunction post HA exposure.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, mice were subjected to a decompression chamber to simulate a 6000-m altitude exposure for 10 days, followed by the other 10-day de-acclimatization period at a lower altitude of 400 m.
Report a problemFND-4165414702
02AnimalAnimal study (in vivo)Mechanism
In mice, MOTS‑c activated the Pink1/Parkin pathway, promoting mitophagy and improving mitochondrial quality.
In plain wordsIn mice, MOTS‑c switched on a cell-cleaning pathway (Pink1/Parkin) and improved mitochondrial quality.
Peptide
MOTS-c
Outcome
IncreasePink1/Parkin pathway, mitophagy and mitochondrial quality
Study
mousen: not reported in source
High-altitude exposure and de-acclimatization model
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Mechanistically, MOTS-c activated the PTEN-induced putative kinase 1 (Pink1)/Parkin pathway, promoting mitophagy and improving mitochondrial quality.
Report a problemFND-4165414703
03AnimalAnimal study (in vivo)Mechanism
In mice, silencing Pink1 abolished the protective effects of MOTS‑c during de-acclimatization.
In plain wordsIn mice, when Pink1 was silenced, MOTS‑c no longer protected the heart during return from high altitude.
Peptide
MOTS-c
Outcome
No significant changeMOTS-c protection with Pink1 silencing
Study
mousen: not reported in source
High-altitude exposure and de-acclimatization model
Comparator
Without Pink1 silencing
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Silencing Pink1 abolished the protective effects of MOTS-c during de-acclimatization.
Report a problemFND-4165414704

Natural levels measured2

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.

04HumanEndogenous levelObservational studyOther
Circulating MOTS‑c levels were reduced in patients with high altitude heart disease and acute coronary syndrome.
In plain wordsPeople with high altitude heart disease or acute coronary syndrome had lower levels of the body's own MOTS‑c in the blood.
Peptide
MOTS-c
Outcome
DecreaseCirculating MOTS-c in high altitude heart disease and acute coronary syndrome
Study
n: not reported in source
Outcome group
Mitochondrial function · Cardiovascular
Source sentences
Summary
Additionally, reduced circulating MOTS-c levels were observed in patients with high altitude heart disease and acute coronary syndrome.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4165414705
05AnimalEndogenous levelAnimal study (in vivo)Other
In mice after high-altitude exposure, cardiac dysfunction persisted through de-acclimatization together with sustained mitochondrial dysfunction and MOTS‑c deficiency.
In plain wordsIn mice, heart problems after high altitude lasted after return to low altitude, together with low levels of the body's own MOTS‑c.
Peptide
MOTS-c
Outcome
DecreaseMOTS-c deficiency after high-altitude exposure
Study
mousen: not reported in source
High-altitude exposure and de-acclimatization model
Outcome group
Mitochondrial function · Cardiovascular
Source sentences
Summary
The cardiac dysfunction induced by HA exposure persisted throughout the de-acclimatization, accompanied with sustained mitochondrial dysfunction and the short peptide mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c) deficiency.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, mice were subjected to a decompression chamber to simulate a 6000-m altitude exposure for 10 days, followed by the other 10-day de-acclimatization period at a lower altitude of 400 m.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4165414701

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.

Publication types

Journal Article

MeSH terms

Keywords

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