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Study · Not a test of the peptide alone · 2027

13 results

Mitochondria-derived peptide hydrogel augments mitochondrial transplantation for promoting cardiac repair via macrophage metabolic reprogramming.

Li H, Zhang Y, Jian Y, Fang F, Ouyang W, Zhuang D, Ju W, Gao R, Gao Y, Kang S, Kong P, Li Y, Pan X, Wang W, Feng Z

Bioactive materials14 Aug 2026

PMID42633281 (opens in a new tab)PMCIDPMC13499492 (opens in a new tab)DOI10.1016/j.bioactmat.2026.06.010 (opens in a new tab)PepBankPUB-42633281
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Summary

Myocardial infarction (MI) is characterized by severe oxidative stress, excessive inflammation, and profound mitochondrial dysfunction. Although mitochondrial transplantation offers therapeutic promise for MI, its clinical translation is severely hampered by the extreme fragility of donor mitochondria with rapid loss of functional viability after isolation. Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI. It has been observed that MQgel significantly extends the survival of isolated mitochondria and maintains metabolic enzyme activity for at least 8 h. More importantly, MQgel not only shields donor mitochondria from oxidative stress and calcium overload, but also enhances mitochondrial internalization by macrophages through an adenosine 5'-monophosphate-activated protein kinase (AMPK)-dependent mechanism. Furthermore, MQgel@Mito facilitates metabolic reprogramming of macrophages by suppressing pro-inflammatory glycolysis and enhancing oxidative phosphorylation (OXPHOS), thereby attenuating M1 polarization. Additionally, MQgel@Mito maintains mitochondrial homeostasis, reduces reactive oxygen species (ROS), and rescues apoptosis of macrophages. In a rat MI model, MQgel@Mito reduces M1 macrophage infiltration and cardiomyocyte damage by delivering viable mitochondria, thereby improving cardiac function and limiting pathological remodeling. These findings establish a paradigm for mitochondrial protection and demonstrate macrophage immunometabolism as a viable therapeutic strategy for MI.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study13

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone13

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.

  1. 01AnimalNot a test of MOTS-c aloneAnimal study (in vivo)Efficacy outcome

    In a rat myocardial infarction model, MQgel@Mito reduced M1 macrophage infiltration.

    In plain wordsIn rats with heart attack, a hydrogel made with MOTS‑c and mitochondria reduced harmful M1 macrophages in the heart.

    Peptide
    MOTS-c
    Outcome
    DecreaseM1 macrophage infiltration
    Study

    ratn: not reported in source

    Myocardial infarction model
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    In a rat MI model, MQgel@Mito reduces M1 macrophage infiltration and cardiomyocyte damage by delivering viable mitochondria, thereby improving cardiac function and limiting pathological remodeling.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  2. 02AnimalNot a test of MOTS-c aloneAnimal study (in vivo)Efficacy outcome

    In a rat myocardial infarction model, MQgel@Mito reduced cardiomyocyte damage.

    In plain wordsIn rats with heart attack, a hydrogel made with MOTS‑c and mitochondria reduced heart muscle cell damage.

    Peptide
    MOTS-c
    Outcome
    DecreaseCardiomyocyte damage
    Study

    ratn: not reported in source

    Myocardial infarction model
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    In a rat MI model, MQgel@Mito reduces M1 macrophage infiltration and cardiomyocyte damage by delivering viable mitochondria, thereby improving cardiac function and limiting pathological remodeling.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  3. 03AnimalNot a test of MOTS-c aloneAnimal study (in vivo)Efficacy outcome

    In a rat myocardial infarction model, MQgel@Mito improved cardiac function.

    In plain wordsIn rats with heart attack, a hydrogel made with MOTS‑c and mitochondria improved heart function.

    Peptide
    MOTS-c
    Outcome
    IncreaseCardiac function
    Study

    ratn: not reported in source

    Myocardial infarction model
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    In a rat MI model, MQgel@Mito reduces M1 macrophage infiltration and cardiomyocyte damage by delivering viable mitochondria, thereby improving cardiac function and limiting pathological remodeling.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  4. 04AnimalNot a test of MOTS-c aloneAnimal study (in vivo)Efficacy outcome

    In a rat myocardial infarction model, MQgel@Mito limited pathological cardiac remodeling.

    In plain wordsIn rats with heart attack, a hydrogel made with MOTS‑c and mitochondria limited harmful changes in heart structure.

    Peptide
    MOTS-c
    Outcome
    DecreasePathological cardiac remodeling
    Study

    ratn: not reported in source

    Myocardial infarction model
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    In a rat MI model, MQgel@Mito reduces M1 macrophage infiltration and cardiomyocyte damage by delivering viable mitochondria, thereby improving cardiac function and limiting pathological remodeling.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  5. 05LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel enhanced the uptake of mitochondria by macrophages through an AMPK-dependent mechanism.

    In plain wordsIn cells, a hydrogel made with MOTS‑c increased the uptake of mitochondria by macrophages through an AMPK-dependent route.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial internalization by macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    enhances mitochondrial internalization by macrophages through an adenosine 5'-monophosphate-activated protein kinase (AMPK)-dependent mechanism
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  6. 06LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito suppressed pro-inflammatory glycolysis in macrophages.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria lowered pro-inflammatory glycolysis in macrophages.

    Peptide
    MOTS-c
    Outcome
    DecreasePro-inflammatory glycolysis in macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    Furthermore, MQgel@Mito facilitates metabolic reprogramming of macrophages by suppressing pro-inflammatory glycolysis and enhancing oxidative phosphorylation (OXPHOS), thereby attenuating M1 polarization.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  7. 07LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito enhanced oxidative phosphorylation in macrophages.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria increased oxidative phosphorylation in macrophages.

    Peptide
    MOTS-c
    Outcome
    IncreaseOxidative phosphorylation (OXPHOS) in macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    Furthermore, MQgel@Mito facilitates metabolic reprogramming of macrophages by suppressing pro-inflammatory glycolysis and enhancing oxidative phosphorylation (OXPHOS), thereby attenuating M1 polarization.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  8. 08LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito attenuated M1 polarization of macrophages.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria reduced M1 polarization of macrophages.

    Peptide
    MOTS-c
    Outcome
    DecreaseM1 polarization of macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Furthermore, MQgel@Mito facilitates metabolic reprogramming of macrophages by suppressing pro-inflammatory glycolysis and enhancing oxidative phosphorylation (OXPHOS), thereby attenuating M1 polarization.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  9. 09LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito maintained mitochondrial homeostasis in macrophages.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria helped keep mitochondria in balance in macrophages.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial homeostasis in macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    Additionally, MQgel@Mito maintains mitochondrial homeostasis, reduces reactive oxygen species (ROS), and rescues apoptosis of macrophages.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  10. 10LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito reduced reactive oxygen species in macrophages.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria lowered reactive oxygen species in macrophages.

    Peptide
    MOTS-c
    Outcome
    DecreaseReactive oxygen species in macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    Additionally, MQgel@Mito maintains mitochondrial homeostasis, reduces reactive oxygen species (ROS), and rescues apoptosis of macrophages.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  11. 11LabNot a test of MOTS-c aloneIn vitro (cells)Mechanism

    MQgel@Mito rescued macrophages from apoptosis.

    In plain wordsIn cells, a hydrogel made with MOTS‑c and mitochondria reduced macrophage cell death.

    Peptide
    MOTS-c
    Outcome
    DecreaseApoptosis of macrophages
    Study

    n: not reported in source

    Macrophages
    Outcome group
    Mitochondrial function · Immune and inflammation

    Source sentences

    Summary
    Additionally, MQgel@Mito maintains mitochondrial homeostasis, reduces reactive oxygen species (ROS), and rescues apoptosis of macrophages.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  12. 12LabNot a test of MOTS-c aloneIn vitro (cell-free)Activity measurement

    In isolated mitochondria, the MOTS‑c-Q11 hydrogel (MQgel) extended mitochondrial survival and kept metabolic enzyme activity for at least 8 h.

    In plain wordsIn lab tests, a hydrogel made with MOTS‑c kept isolated mitochondria alive and working longer.

    Peptide
    MOTS-c
    Outcome
    IncreaseSurvival of isolated mitochondria and metabolic enzyme activity
    Study

    n: not reported in source

    Isolated donor mitochondria
    Outcome group
    Mitochondrial function · Cardiovascular

    Measurements

    Duration of maintained enzyme activity
    ≥ 8 h
    MQgel

    Source sentences

    Summary
    It has been observed that MQgel significantly extends the survival of isolated mitochondria and maintains metabolic enzyme activity for at least 8 h.
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

  13. 13LabNot a test of MOTS-c aloneIn vitro (cell-free)Activity measurement

    MQgel shielded donor mitochondria from oxidative stress and calcium overload.

    In plain wordsIn lab tests, a hydrogel made with MOTS‑c protected donor mitochondria from oxidative stress and calcium overload.

    Peptide
    MOTS-c
    Outcome
    DecreaseProtection of donor mitochondria from oxidative stress and calcium overload
    Study

    n: not reported in source

    Isolated donor mitochondria
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    MQgel not only shields donor mitochondria from oxidative stress and calcium overload
    1 context sentence
    Summary · context
    Here, inspired by the intrinsic cellular defense mechanisms against mitochondrial dysfunction, MOTS-c, a mitochondria-derived peptide (MDP), is selected and further conjugated with self-assembling peptide (Q11) to fabricate a hydrogel-based mitochondrial delivery system (MQgel@Mito) for cardiac repair after MI.

    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.

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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