MOTS-c Protects Against Acetaminophen-induced Liver Injury through the MAPK Signaling Pathway.

Li N, Xu Y, Chen Q, Jiang J, Li WW

Protein and peptide letters1 Jan 2026

PMID41764620DOI10.2174/0109298665430028251230103831PepBankPUB-41764620

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 study19

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with acetaminophen-induced liver injury, MOTS‑c attenuated the increase in AST.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced the rise in the liver enzyme AST.
Peptide
MOTS-c
Outcome
DecreaseAST level
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Administration of MOTS-c via i.p. injection markedly attenuated APAP-induced increases in AST and ALT levels, histopathological liver damage, and other liver injury markers.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462003
02AnimalAnimal study (in vivo)Efficacy outcome
In mice with acetaminophen-induced liver injury, MOTS‑c attenuated the increase in ALT.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced the rise in the liver enzyme ALT.
Peptide
MOTS-c
Outcome
DecreaseALT level
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Administration of MOTS-c via i.p. injection markedly attenuated APAP-induced increases in AST and ALT levels, histopathological liver damage, and other liver injury markers.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462004
03AnimalAnimal study (in vivo)Efficacy outcome
In mice with acetaminophen-induced liver injury, MOTS‑c attenuated histopathological liver damage.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced visible liver tissue damage.
Peptide
MOTS-c
Outcome
DecreaseHistopathological liver damage
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Administration of MOTS-c via i.p. injection markedly attenuated APAP-induced increases in AST and ALT levels, histopathological liver damage, and other liver injury markers.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462005
04AnimalAnimal study (in vivo)Efficacy outcome
In mice with acetaminophen-induced liver injury, MOTS‑c attenuated other liver injury markers.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced other signs of liver injury.
Peptide
MOTS-c
Outcome
DecreaseOther liver injury markers
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Administration of MOTS-c via i.p. injection markedly attenuated APAP-induced increases in AST and ALT levels, histopathological liver damage, and other liver injury markers.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462006
05AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c suppressed the release of TNF-α.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered the inflammation signal TNF-α.
Peptide
MOTS-c
Outcome
DecreaseTNF-α
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
MOTS-c treatment suppressed the release of pro-inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) and macrophage infiltration induced by APAP.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462007
06AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c suppressed the release of IL-1β.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered the inflammation signal IL-1β.
Peptide
MOTS-c
Outcome
DecreaseIL-1β
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
MOTS-c treatment suppressed the release of pro-inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) and macrophage infiltration induced by APAP.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462008
07AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c suppressed the release of IL-6.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered the inflammation signal IL-6.
Peptide
MOTS-c
Outcome
DecreaseIL-6
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
MOTS-c treatment suppressed the release of pro-inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) and macrophage infiltration induced by APAP.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462009
08AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c suppressed the release of COX-2.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered the inflammation signal COX-2.
Peptide
MOTS-c
Outcome
DecreaseCOX-2
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
MOTS-c treatment suppressed the release of pro-inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) and macrophage infiltration induced by APAP.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462010
09AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c suppressed macrophage infiltration.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced the arrival of immune cells called macrophages in the liver.
Peptide
MOTS-c
Outcome
DecreaseMacrophage infiltration
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
MOTS-c treatment suppressed the release of pro-inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) and macrophage infiltration induced by APAP.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462011
10AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c restored GSH content.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c restored the level of the antioxidant GSH.
Peptide
MOTS-c
Outcome
IncreaseGlutathione (GSH) content
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Furthermore, MOTS-c treatment significantly restored GSH content, diminished reactive oxygen species (ROS) production, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462012
11AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c diminished reactive oxygen species production.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered the production of reactive oxygen molecules.
Peptide
MOTS-c
Outcome
DecreaseReactive oxygen species production
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Furthermore, MOTS-c treatment significantly restored GSH content, diminished reactive oxygen species (ROS) production, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462013
12AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c diminished oxidative stress.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c lowered oxidative stress.
Peptide
MOTS-c
Outcome
DecreaseOxidative stress
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Furthermore, MOTS-c treatment significantly restored GSH content, diminished reactive oxygen species (ROS) production, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462014
13AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c significantly attenuated the increase in apoptosis shown by TUNEL staining.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced the rise in liver cell death.
Peptide
MOTS-c
Outcome
DecreaseHepatocyte apoptosis (TUNEL)
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
TUNEL staining confirmed that increased apoptosis in APAPtreated livers was significantly attenuated by MOTS-c, which are key contributors to hepatocyte death and liver injury.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462015
14AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c inhibited APAP-induced phosphorylation of ERK.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced activation of the ERK signal.
Peptide
MOTS-c
Outcome
DecreaseERK phosphorylation
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Receptor activity and mechanism · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistic studies revealed that MOTS-c inhibited APAP-induced phosphorylation of MAPK pathway components, including ERK, JNK, and p38.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462016
15AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c inhibited APAP-induced phosphorylation of JNK.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced activation of the JNK signal.
Peptide
MOTS-c
Outcome
DecreaseJNK phosphorylation
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Receptor activity and mechanism · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistic studies revealed that MOTS-c inhibited APAP-induced phosphorylation of MAPK pathway components, including ERK, JNK, and p38.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462017
16AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, MOTS‑c inhibited APAP-induced phosphorylation of p38.
In plain wordsIn mice with acetaminophen liver injury, MOTS‑c reduced activation of the p38 signal.
Peptide
MOTS-c
Outcome
Decreasep38 phosphorylation
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Receptor activity and mechanism · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistic studies revealed that MOTS-c inhibited APAP-induced phosphorylation of MAPK pathway components, including ERK, JNK, and p38.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462018
17AnimalAnimal study (in vivo)Mechanism
In mice with acetaminophen-induced liver injury, co-treatment with ERK, JNK and p38 inhibitors abolished the protective effect of MOTS‑c on serum ALT and AST.
In plain wordsIn mice with acetaminophen liver injury, blocking the ERK, JNK and p38 signals removed the protection MOTS‑c gave on liver enzymes.
Peptide
MOTS-c
Outcome
No significant changeMOTS-c protection with ERK, JNK and p38 inhibitors
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Outcome group
Liver fat and liver function · Liver
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
The protective effects of MOTS-c on serum ALT and AST levels were abolished by co-treatment with inhibitors of ERK, JNK, and p38.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
Report a problemFND-4176462019

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.

18AnimalEndogenous levelAnimal study (in vivo)Other
In mice with acetaminophen-induced liver injury, the body's own plasma MOTS‑c was lower than in controls.
In plain wordsIn mice with acetaminophen liver injury, the body's own MOTS‑c in blood was lower than in controls.
Peptide
MOTS-c
Outcome
DecreasePlasma MOTS-c in acetaminophen liver injury
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Comparator
Controls
Outcome group
Liver fat and liver function · Liver
Source sentences
Summary
MOTS-c levels in both plasma and liver tissues were significantly reduced in APAPinduced AILI mice compared with controls.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4176462001
19AnimalEndogenous levelAnimal study (in vivo)Other
In mice with acetaminophen-induced liver injury, the body's own MOTS‑c in liver tissue was lower than in controls.
In plain wordsIn mice with acetaminophen liver injury, the body's own MOTS‑c in liver tissue was lower than in controls.
Peptide
MOTS-c
Outcome
DecreaseLiver tissue MOTS-c in acetaminophen liver injury
Study
mousen: not reported in source
Acetaminophen-induced liver injury
Comparator
Controls
Outcome group
Liver fat and liver function · Liver
Source sentences
Summary
MOTS-c levels in both plasma and liver tissues were significantly reduced in APAPinduced AILI mice compared with controls.
1 context sentence(design, population, supporting numbers)
Summary · context
An AILI model was established in male C57BL/6 mice via intraperitoneal (i.p.) injection of APAP (300 mg/kg).
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-4176462002

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
9 Oct 2026, 18:17 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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