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Study · In vitro (cells) · 2020

2 results

Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction.

Liang Q, Cai M, Zhang J, Song W, Zhu W, Xi L, Tian Z

International journal of molecular sciences23 Sept 2020Cited by 27 (Europe PMC)

PMID32977624 (opens in a new tab)PMCIDPMC7582695 (opens in a new tab)DOI10.3390/ijms21197010 (opens in a new tab)PepBankPUB-32977624
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Summary

Pathological remodeling is the main detrimental complication after myocardial infarction (MI). Overproduction of reactive oxygen species (ROS) in infarcted myocardium may contribute to this process. Adequate exercise training after MI may reduce oxidative stress-induced cardiac tissue damage and remodeling. SET and MYND domain containing 1 (Smyd1) is a muscle-specific histone methyltransferase which is upregulated by resistance training, may strengthen sarcomere assembly and myofiber folding, and may promote skeletal muscles growth and hypertrophy. However, it remains elusive if Smyd1 has similar functions in post-MI cardiac muscle and participates in exercise-induced cardioprotection. Accordingly, we investigated the effects of interval treadmill exercise on cardiac function, ROS generation, Smyd1 expression, and sarcomere assembly of F-actin in normal and infarcted hearts. Adult male rats were randomly divided into five groups (n = 10/group): control (C), exercise alone (EX), sham-operated (S), MI induced by permanent ligation of left anterior descending coronary artery (MI), and MI with interval exercise training (MI + EX). Exercise training significantly improved post-MI cardiac function and sarcomere assembly of F-actin. The cardioprotective effects were associated with increased Smyd1, Trx1, cTnI, and α-actinin expression as well as upregulated ratio of phosphorylated AMP-activated protein kinase (AMPK)/AMPK, whereas Hsp90, MuRF1, brain natriuretic peptide (BNP) expression, ROS generation, and myocardial fibrosis were attenuated. The improved post-MI cardiac function was associated with increased Smyd1 expression. In cultured H9C2 cardiomyoblasts, in vitro treatment with H2O2 (50 µmol/L) or AMP-activated protein kinase (AMPK) agonist (AICAR, 1 mmol/L) or their combination for 4 h simulated the effects of exercise on levels of ROS and Smyd1. In conclusion, we demonstrated a novel role of Smyd1 in association with post-MI exercise-induced cardioprotection. The moderate level of ROS-induced upregulation of Smyd1 may be an important target for modulating post-MI cardiac function and remodeling.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01LabIn vitro (cells)Mechanism

    In cultured H9C2 cardiomyoblasts, AICAR treatment simulated exercise effects on ROS levels.

    In plain wordsIn cells, AICAR treatment reproduced exercise-related effects on reactive oxygen levels.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedROS levels
    Study

    n: not reported in source

    cultured H9C2 cardiomyoblasts
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    1 mmol/L · 4 hAs given in this study.

    Source sentences

    Summary
    In cultured H9C2 cardiomyoblasts, in vitro treatment with H2O2 (50 µmol/L) or AMP-activated protein kinase (AMPK) agonist (AICAR, 1 mmol/L) or their combination for 4 h simulated the effects of exercise on levels of ROS and Smyd1.
  2. 02LabIn vitro (cells)Mechanism

    In cultured H9C2 cardiomyoblasts, AICAR treatment simulated exercise effects on Smyd1 levels.

    In plain wordsIn cells, AICAR treatment reproduced exercise-related effects on Smyd1 levels.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedSmyd1 levels
    Study

    n: not reported in source

    cultured H9C2 cardiomyoblasts
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    1 mmol/L · 4 hAs given in this study.

    Source sentences

    Summary
    In cultured H9C2 cardiomyoblasts, in vitro treatment with H2O2 (50 µmol/L) or AMP-activated protein kinase (AMPK) agonist (AICAR, 1 mmol/L) or their combination for 4 h simulated the effects of exercise on levels of ROS and Smyd1.

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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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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