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Study · Animal study (in vivo) · mouse · 2026

26 results

Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.

Liao Y, Xu J, Jiao Y, Sun X, Gao M, Ding Y, Cai D, Shen Y, Zhou X, Han W

Biomedicines5 May 2026

PMID42193373 (opens in a new tab)PMCIDPMC13204372 (opens in a new tab)DOI10.3390/biomedicines14051048 (opens in a new tab)PepBankPUB-42193373
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Summary

Background: Atrial fibrillation (AF) is a common clinical arrhythmia associated with mitochondrial dysfunction, oxidative stress, and atrial fibrosis. Mitochondrial-derived peptides (MDPs), including humanin (HN) and MOTS-c, exhibit cytoprotective properties, but their role in AF remains largely unknown. Objective: This study aimed to investigate the expression of HN and MOTS-c in AF patients and to evaluate their therapeutic potential and underlying mechanisms in an AngII-induced mouse model and primary cardiac cells. Methods: HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence. Plasma levels were measured in a matched cohort (39 AF patients, 39 sinus rhythm controls). Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c. Results: HN and MOTS-c were significantly downregulated in human AF atrial tissue, and their levels inversely correlated with fibrosis extent. Plasma MOTS-c was decreased in AF patients and inversely correlated with NT-proBNP. In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy. Peptide treatment was associated with improved mitochondrial ultrastructure, reduced mitochondrial fission proteins (Drp1, Fis1), and lower pro-inflammatory cytokines (IL-1β, IL-6) in mouse atria. In primary cardiomyocytes, both peptides mitigated AngII-induced oxidative stress. In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration. Exploratory RNA-seq suggested that HNG predominantly affects cell adhesion pathways, while MOTS-c acts on metabolic processes. Conclusions: Downregulation of HN and MOTS-c in human AF is associated with disease severity. In murine models, HNG or MOTS-c administration attenuates atrial fibrosis and mitochondrial dysfunction and reduces AF inducibility. These findings suggest that MDPs may represent a novel therapeutic avenue for AF, although further validation with larger cohorts and mechanistic studies are required.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study26

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with AngII-induced atrial fibrillation, treatment with the humanin analogue HNG reduced AF inducibility.

    In plain wordsIn mice, a humanin analogue made atrial fibrillation less easy to trigger.

    Peptide
    Humanin
    Outcome
    DecreaseAF inducibility
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with AngII-induced atrial fibrillation, HNG attenuated atrial fibrosis.

    In plain wordsIn mice, a humanin analogue reduced scarring of the heart atria caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAtrial fibrosis
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with AngII-induced atrial fibrillation, HNG attenuated atrial hypertrophy.

    In plain wordsIn mice, a humanin analogue reduced the heart atrial enlargement caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAtrial hypertrophy
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with AngII-induced atrial fibrillation, peptide treatment was associated with improved mitochondrial ultrastructure in atria.

    In plain wordsIn mice, peptide treatment was linked to better-looking mitochondria in heart atria.

    Peptide
    Humanin
    Outcome
    IncreaseMitochondrial ultrastructure in atria
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Peptide treatment was associated with improved mitochondrial ultrastructure
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with AngII-induced atrial fibrillation, peptide treatment was associated with reduced mitochondrial fission proteins Drp1 and Fis1 in atria.

    In plain wordsIn mice, peptide treatment was linked to lower levels of two mitochondrial fission proteins in heart atria.

    Peptide
    Humanin
    Outcome
    DecreaseMitochondrial fission proteins (Drp1, Fis1)
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    reduced mitochondrial fission proteins (Drp1, Fis1)
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with AngII-induced atrial fibrillation, peptide treatment was associated with lower IL-1β and IL-6 in atria.

    In plain wordsIn mice, peptide treatment was linked to lower inflammatory cytokines in heart atria.

    Peptide
    Humanin
    Outcome
    DecreasePro-inflammatory cytokines (IL-1β, IL-6) in atria
    Study

    mousen = 36

    AngII-induced mouse model of atrial fibrillation
    Comparator
    AngII alone
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    lower pro-inflammatory cytokines (IL-1β, IL-6) in mouse atria.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In AngII-exposed mice, MOTS‑c (reported alongside HNG) reduced atrial fibrillation inducibility.

    In plain wordsIn mice with induced atrial fibrillation, MOTS‑c treatment made the arrhythmia less easy to trigger.

    Peptide
    MOTS-c
    Outcome
    DecreaseAF inducibility
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In AngII-exposed mice, MOTS‑c (reported alongside HNG) attenuated AngII-induced atrial fibrosis.

    In plain wordsIn mice, MOTS‑c treatment reduced scarring (fibrosis) in the heart atria caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAtrial fibrosis
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  9. 09AnimalAnimal study (in vivo)Efficacy outcome

    In AngII-exposed mice, MOTS‑c (reported alongside HNG) attenuated AngII-induced atrial hypertrophy.

    In plain wordsIn mice, MOTS‑c treatment reduced the atrial enlargement caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAtrial hypertrophy
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In mouse atria, peptide treatment (HNG or MOTS‑c) was associated with improved mitochondrial ultrastructure.

    In plain wordsIn mice, treatment with these peptides was linked to healthier mitochondria in the heart atria.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial ultrastructure in mouse atria
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Peptide treatment was associated with improved mitochondrial ultrastructure
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In mouse atria, peptide treatment (HNG or MOTS‑c) was associated with lower mitochondrial fission proteins Drp1 and Fis1.

    In plain wordsIn mice, treatment with these peptides was linked to lower levels of proteins that split mitochondria.

    Peptide
    MOTS-c
    Outcome
    DecreaseMitochondrial fission proteins (Drp1, Fis1)
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    reduced mitochondrial fission proteins (Drp1, Fis1)
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  12. 12AnimalAnimal study (in vivo)Mechanism

    In mouse atria, peptide treatment (HNG or MOTS‑c) was associated with lower IL-1β and IL-6.

    In plain wordsIn mice, treatment with these peptides was linked to lower inflammation signals in the heart atria.

    Peptide
    MOTS-c
    Outcome
    DecreasePro-inflammatory cytokines (IL-1β, IL-6) in mouse atria
    Study

    mousen: not reported in source

    AngII-induced atrial fibrillation
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    lower pro-inflammatory cytokines (IL-1β, IL-6) in mouse atria
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  13. 13LabIn vitro (cells)Mechanism

    In primary rat cardiomyocytes, MOTS‑c (with HNG) mitigated AngII-induced oxidative stress.

    In plain wordsIn rat heart muscle cells in the lab, MOTS‑c reduced the oxidative stress caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAngII-induced oxidative stress in cardiomyocytes
    Study

    ratn: not reported in source

    Primary cardiomyocytes
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In primary cardiomyocytes, both peptides mitigated AngII-induced oxidative stress.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  14. 14LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, MOTS‑c (with HNG) inhibited AngII-induced activation.

    In plain wordsIn rat heart fibroblasts in the lab, MOTS‑c blocked the activation caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAngII-induced fibroblast activation
    Study

    ratn: not reported in source

    Primary cardiac fibroblasts
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  15. 15LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, MOTS‑c (with HNG) inhibited AngII-induced proliferation.

    In plain wordsIn rat heart fibroblasts in the lab, MOTS‑c reduced the growth caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAngII-induced fibroblast proliferation
    Study

    ratn: not reported in source

    Primary cardiac fibroblasts
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  16. 16LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, MOTS‑c (with HNG) inhibited AngII-induced migration.

    In plain wordsIn rat heart fibroblasts in the lab, MOTS‑c reduced the cell movement caused by angiotensin II.

    Peptide
    MOTS-c
    Outcome
    DecreaseAngII-induced fibroblast migration
    Study

    ratn: not reported in source

    Primary cardiac fibroblasts
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  17. 17LabIn vitro (cells)Mechanism

    In primary rat cardiomyocytes, the humanin analogue mitigated AngII-induced oxidative stress.

    In plain wordsIn rat heart cells in the lab, a humanin analogue reduced oxidative stress caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAngII-induced oxidative stress in cardiomyocytes
    Study

    ratn: not reported in source

    Primary rat cardiomyocytes exposed to AngII
    Comparator
    AngII alone
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In primary cardiomyocytes, both peptides mitigated AngII-induced oxidative stress.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  18. 18LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, the peptides directly inhibited AngII-induced activation.

    In plain wordsIn rat heart fibroblasts in the lab, the peptides directly reduced activation caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAngII-induced fibroblast activation
    Study

    ratn: not reported in source

    Primary rat cardiac fibroblasts exposed to AngII
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  19. 19LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, the peptides directly inhibited AngII-induced proliferation.

    In plain wordsIn rat heart fibroblasts in the lab, the peptides directly reduced growth caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAngII-induced fibroblast proliferation
    Study

    ratn: not reported in source

    Primary rat cardiac fibroblasts exposed to AngII
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.
  20. 20LabIn vitro (cells)Mechanism

    In primary rat cardiac fibroblasts, the peptides directly inhibited AngII-induced migration.

    In plain wordsIn rat heart fibroblasts in the lab, the peptides directly reduced cell movement caused by angiotensin II.

    Peptide
    Humanin
    Outcome
    DecreaseAngII-induced fibroblast migration
    Study

    ratn: not reported in source

    Primary rat cardiac fibroblasts exposed to AngII
    Comparator
    AngII alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration.
    1 context sentence
    Summary · context
    Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c.

Natural levels measured6

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.

  1. 21HumanEndogenous levelObservational studyOther

    Plasma MOTS‑c was lower in patients with atrial fibrillation than in sinus rhythm controls.

    In plain wordsPeople with atrial fibrillation had lower levels of the body's own MOTS‑c in blood than people with normal rhythm.

    Peptide
    MOTS-c
    Outcome
    DecreasePlasma MOTS-c in atrial fibrillation
    Study

    n = 78

    Comparator
    Sinus rhythm controls
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Plasma MOTS-c was decreased in AF patients and inversely correlated with NT-proBNP.
    1 context sentence
    Summary · context
    Plasma levels were measured in a matched cohort (39 AF patients, 39 sinus rhythm controls).

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  2. 22HumanEndogenous levelObservational studyOther

    In patients with atrial fibrillation, plasma MOTS‑c was inversely correlated with NT-proBNP.

    In plain wordsLower natural MOTS‑c in blood was linked to higher NT-proBNP, a heart strain marker, in people with atrial fibrillation.

    Peptide
    MOTS-c
    Outcome
    Not applicableAssociation of plasma MOTS-c with NT-proBNP
    Study

    n = 78

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Plasma MOTS-c was decreased in AF patients and inversely correlated with NT-proBNP.
    1 context sentence
    Summary · context
    Plasma levels were measured in a matched cohort (39 AF patients, 39 sinus rhythm controls).

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  3. 23HumanEndogenous levelObservational studyOther

    In atrial tissue from patients with atrial fibrillation, MOTS‑c expression was downregulated.

    In plain wordsIn people with atrial fibrillation, the body's own MOTS‑c was lower in heart atrial tissue.

    Peptide
    MOTS-c
    Outcome
    DecreaseMOTS-c expression in atrial tissue
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    HN and MOTS-c were significantly downregulated in human AF atrial tissue, and their levels inversely correlated with fibrosis extent.
    1 context sentence
    Summary · context
    HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  4. 24HumanEndogenous levelObservational studyOther

    In human atrial tissue, MOTS‑c levels were inversely correlated with the extent of fibrosis.

    In plain wordsIn human heart tissue, lower natural MOTS‑c levels were linked to more fibrosis.

    Peptide
    MOTS-c
    Outcome
    Not applicableAssociation of atrial MOTS-c with fibrosis extent
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    HN and MOTS-c were significantly downregulated in human AF atrial tissue, and their levels inversely correlated with fibrosis extent.
    1 context sentence
    Summary · context
    HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  5. 25HumanEndogenous levelObservational studyOther

    In human atrial fibrillation atrial tissue, the body's own humanin was downregulated.

    In plain wordsIn people with atrial fibrillation, the body's own humanin was lower in heart atrial tissue.

    Peptide
    Humanin
    Outcome
    DecreaseHumanin expression in atrial tissue of AF patients
    Study

    n: not reported in source

    Outcome group
    Endogenous peptide levels · Cardiovascular

    Source sentences

    Summary
    HN and MOTS-c were significantly downregulated in human AF atrial tissue, and their levels inversely correlated with fibrosis extent.
    1 context sentence
    Summary · context
    HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

  6. 26HumanEndogenous levelObservational studyOther

    In human atrial fibrillation atrial tissue, humanin levels correlated inversely with the extent of fibrosis.

    In plain wordsIn people with atrial fibrillation, lower natural humanin levels in heart tissue were linked to more fibrosis.

    Peptide
    Humanin
    Outcome
    Not applicableHumanin level and atrial fibrosis extent
    Study

    n: not reported in source

    Outcome group
    Endogenous peptide levels · Cardiovascular

    Source sentences

    Summary
    their levels inversely correlated with fibrosis extent.
    1 context sentence
    Summary · context
    HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

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. Versions 4 to 18Current

    28 Oct 2026, 02:02 UTC

    The same notice was added 15 times, first on 13 Oct 2026, 21:44 UTC. The status did not change between them.

    Study results updated

  2. Version 3

    13 Oct 2026, 16:31 UTC

    Study data updated · source update from Europe PMC

  3. Version 2

    10 Oct 2026, 08:19 UTC

    Study results updated

  4. 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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