Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury: experimental and in silico evidence from rat heart models.

Santhanam SS, Jayaraman S, Kurian GA

Naunyn-Schmiedeberg's archives of pharmacology28 Jan 2026

PMID41593376DOI10.1007/s00210-026-05018-0PepBankPUB-41593376

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 study25

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

01LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c at 0.5 mg per kg reduced infarct size by 73% compared with ischemia-reperfusion alone.
In plain wordsIn isolated rat hearts, MOTS‑c at the best dose cut the size of the injured heart area compared with injury alone.
Peptide
MOTS-c
Outcome
DecreaseInfarct size
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.5 mg per kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Measurements
Infarct size reduction
73%
0.5 mg per kg vs ischemia-reperfusion alone
Source sentences
Summary
MOTS-c at 0.5 mg per kg conferred maximal protection, producing a 73% reduction in infarct size compared with ischemia-reperfusion alone, improving heart rate, left ventricular developed pressure, and rate-pressure product, and lowering end-diastolic pressure.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337601
02LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c at 0.5 mg per kg improved heart rate compared with ischemia-reperfusion alone.
In plain wordsIn isolated rat hearts, MOTS‑c at the best dose improved heart rate compared with injury alone.
Peptide
MOTS-c
Outcome
IncreaseHeart rate
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.5 mg per kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
MOTS-c at 0.5 mg per kg conferred maximal protection, producing a 73% reduction in infarct size compared with ischemia-reperfusion alone, improving heart rate, left ventricular developed pressure, and rate-pressure product, and lowering end-diastolic pressure.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337602
03LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c at 0.5 mg per kg improved left ventricular developed pressure compared with ischemia-reperfusion alone.
In plain wordsIn isolated rat hearts, MOTS‑c at the best dose improved the pressure the heart made, compared with injury alone.
Peptide
MOTS-c
Outcome
IncreaseLeft ventricular developed pressure
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.5 mg per kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
MOTS-c at 0.5 mg per kg conferred maximal protection, producing a 73% reduction in infarct size compared with ischemia-reperfusion alone, improving heart rate, left ventricular developed pressure, and rate-pressure product, and lowering end-diastolic pressure.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337603
04LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c at 0.5 mg per kg improved rate-pressure product compared with ischemia-reperfusion alone.
In plain wordsIn isolated rat hearts, MOTS‑c at the best dose improved a measure of heart work, compared with injury alone.
Peptide
MOTS-c
Outcome
IncreaseRate-pressure product
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.5 mg per kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
MOTS-c at 0.5 mg per kg conferred maximal protection, producing a 73% reduction in infarct size compared with ischemia-reperfusion alone, improving heart rate, left ventricular developed pressure, and rate-pressure product, and lowering end-diastolic pressure.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337604
05LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c at 0.5 mg per kg lowered end-diastolic pressure compared with ischemia-reperfusion alone.
In plain wordsIn isolated rat hearts, MOTS‑c at the best dose lowered the filling pressure of the heart, compared with injury alone.
Peptide
MOTS-c
Outcome
DecreaseEnd-diastolic pressure
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.5 mg per kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
MOTS-c at 0.5 mg per kg conferred maximal protection, producing a 73% reduction in infarct size compared with ischemia-reperfusion alone, improving heart rate, left ventricular developed pressure, and rate-pressure product, and lowering end-diastolic pressure.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337605
06LabEx vivo tissueEfficacy outcome
In isolated rat hearts, MOTS‑c decreased lactate dehydrogenase release by 65%.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the release of lactate dehydrogenase, a sign of cell damage, compared with injury alone.
Peptide
MOTS-c
Outcome
DecreaseLactate dehydrogenase release
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Heart function · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Measurements
LDH release decrease
65%
MOTS-c vs ischemia-reperfusion alone
Source sentences
Summary
Lactate dehydrogenase release decreased by 65%.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337606
07LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased superoxide dismutase.
In plain wordsIn isolated rat hearts, MOTS‑c raised the antioxidant enzyme superoxide dismutase.
Peptide
MOTS-c
Outcome
IncreaseSuperoxide dismutase
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
Antioxidant defenses improved with increased superoxide dismutase, catalase, and glutathione redox ratio, along with reduced lipid peroxidation.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337607
08LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased catalase.
In plain wordsIn isolated rat hearts, MOTS‑c raised the antioxidant enzyme catalase.
Peptide
MOTS-c
Outcome
IncreaseCatalase
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
Antioxidant defenses improved with increased superoxide dismutase, catalase, and glutathione redox ratio, along with reduced lipid peroxidation.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337608
09LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased the glutathione redox ratio.
In plain wordsIn isolated rat hearts, MOTS‑c improved the glutathione redox ratio, an antioxidant measure.
Peptide
MOTS-c
Outcome
IncreaseGlutathione redox ratio
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
Antioxidant defenses improved with increased superoxide dismutase, catalase, and glutathione redox ratio, along with reduced lipid peroxidation.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337609
10LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c reduced lipid peroxidation.
In plain wordsIn isolated rat hearts, MOTS‑c reduced damage to fats by oxidation.
Peptide
MOTS-c
Outcome
DecreaseLipid peroxidation
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
Antioxidant defenses improved with increased superoxide dismutase, catalase, and glutathione redox ratio, along with reduced lipid peroxidation.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337610
11LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c normalized myeloperoxidase activity.
In plain wordsIn isolated rat hearts, MOTS‑c brought myeloperoxidase, an inflammation enzyme, back to normal.
Peptide
MOTS-c
Outcome
DecreaseMyeloperoxidase activity
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
Myeloperoxidase activity normalized
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337611
12LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c downregulated caspase 3.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the activity of the cell-death gene caspase 3.
Peptide
MOTS-c
Outcome
DecreaseCaspase 3 expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
pro-apoptotic genes including caspase 3, caspase 7, caspase 9, BAX, and PARP were downregulated, while cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337612
13LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c downregulated caspase 7.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the activity of the cell-death gene caspase 7.
Peptide
MOTS-c
Outcome
DecreaseCaspase 7 expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
pro-apoptotic genes including caspase 3, caspase 7, caspase 9, BAX, and PARP were downregulated, while cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337613
14LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c downregulated caspase 9.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the activity of the cell-death gene caspase 9.
Peptide
MOTS-c
Outcome
DecreaseCaspase 9 expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
pro-apoptotic genes including caspase 3, caspase 7, caspase 9, BAX, and PARP were downregulated, while cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337614
15LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c downregulated BAX.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the activity of the cell-death gene BAX.
Peptide
MOTS-c
Outcome
DecreaseBAX expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
pro-apoptotic genes including caspase 3, caspase 7, caspase 9, BAX, and PARP were downregulated, while cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337615
16LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c downregulated PARP.
In plain wordsIn isolated rat hearts, MOTS‑c lowered the activity of the cell-death gene PARP.
Peptide
MOTS-c
Outcome
DecreasePARP expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
pro-apoptotic genes including caspase 3, caspase 7, caspase 9, BAX, and PARP were downregulated, while cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337616
17LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased the cytoprotective gene BCL2.
In plain wordsIn isolated rat hearts, MOTS‑c raised the activity of the protective gene BCL2.
Peptide
MOTS-c
Outcome
IncreaseBCL2 expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337617
18LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased the cytoprotective gene GPX4.
In plain wordsIn isolated rat hearts, MOTS‑c raised the activity of the protective gene GPX4.
Peptide
MOTS-c
Outcome
IncreaseGPX4 expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337618
19LabEx vivo tissueMechanism
In isolated rat hearts, MOTS‑c increased the cytoprotective gene FOXO.
In plain wordsIn isolated rat hearts, MOTS‑c raised the activity of the protective gene FOXO.
Peptide
MOTS-c
Outcome
IncreaseFOXO expression
Study
ratn: not reported in source
Langendorff-perfused isolated heart, ischemia-reperfusion
Comparator
Ischemia-reperfusion alone
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.25-0.7 mg/kg · Krebs-Henseleit buffer perfusion · first 10 min of reperfusionAs given in this study (rat).
Source sentences
Summary
cytoprotective genes including BCL2, GPX4, and FOXO were increased.
1 context sentence(design, population, supporting numbers)
Summary · context
Isolated Langendorff-perfused rat hearts underwent 30-min global ischemia and 60-min reperfusion with or without MOTS-c (0.25-0.7 mg/kg) delivered via Krebs-Henseleit buffer during the first 10 min of reperfusion.
Report a problemFND-4159337619

Studies that did not test the peptide alone6

In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking MOTS-c.

20Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with MAPK.
In plain wordsA computer model predicted that MOTS‑c binds tightly to MAPK. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to MAPK
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337620
21Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with mTOR.
In plain wordsA computer model predicted that MOTS‑c binds tightly to mTOR. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to mTOR
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337621
22Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with AMPK.
In plain wordsA computer model predicted that MOTS‑c binds tightly to AMPK. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to AMPK
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337622
23Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with NRF2.
In plain wordsA computer model predicted that MOTS‑c binds tightly to NRF2. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to NRF2
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337623
24Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with PI3K.
In plain wordsA computer model predicted that MOTS‑c binds tightly to PI3K. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to PI3K
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337624
25Computer modelNot a test of MOTS-c aloneIn silicoActivity measurement
Molecular docking predicted a high-affinity interaction of MOTS‑c with caspase 3.
In plain wordsA computer model predicted that MOTS‑c binds tightly to caspase 3. This is a prediction only.
Peptide
MOTS-c
Outcome
Not applicablePredicted binding to caspase 3
Study
n: not reported in source
Molecular docking
Outcome group
Receptor activity and mechanism · Pharmacology
Source sentences
Summary
Molecular docking demonstrated high-affinity interactions of MOTS-c with MAPK, mTOR, AMPK, NRF2, PI3K, and caspase 3.
In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.
Report a problemFND-4159337625

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

PepBank is a research reference. Talk to a doctor before you use any peptide.

Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury: experimental and in silico evidence from rat heart models.

Summary

Results from this study25

Studies that did not test the peptide alone6

Version history

Subjects

Publication types

MeSH terms

Keywords