ArticleMolecular and cellular biochemistry2015
Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- The relationship between homocysteine and new-onset atrial fibrillation in patients with acute myocardial infarction.Annals of medicine · 2025Article
- Transsulfuration Pathway Products and HInternational journal of molecular sciences · 2025Review
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Review
- The Role of Gasotransmitter-Dependent Signaling Mechanisms in Apoptotic Cell Death in Cardiovascular, Rheumatic, Kidney, and Neurodegenerative Diseases and Mental Disorders.International journal of molecular sciences · 2023Review
- The Functional Interplay between Ethylene, Hydrogen Sulfide, and Sulfur in Plant Heat Stress Tolerance.Biomolecules · 2022Review
- Endoplasmic reticulum stress mediates homocysteine-induced hypertrophy of cardiac cells through activation of cyclic nucleotide phosphodiesterase 1C.Acta biochimica et biophysica Sinica · 2022Article
- miR-195-3p alleviates homocysteine-mediated atherosclerosis by targeting IL-31 through its epigenetics modifications.Aging cell · 2021Article
- The Cardiovascular Effects of Hydrogen Sulfide: The Epigenetic Mechanisms.Advances in experimental medicine and biology · 2021Article
- MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
- Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair.Redox biology · 2020Review
- The role of the gasotransmitter hydrogen sulfide in pathological calcification.British journal of pharmacology · 2020Review
- Hydrogen sulfide lowers hyperhomocysteinemia dependent on cystathionine γ lyase S-sulfhydration in ApoE-knockout atherosclerotic mice.British journal of pharmacology · 2019Article
- Hydrogen Sulfide (HFrontiers in pharmacology · 2018Review
- Exogenous Hydrogen Sulfide Supplement Attenuates Isoproterenol-Induced Myocardial Hypertrophy in a Sirtuin 3-Dependent Manner.Oxidative medicine and cellular longevity · 2018Article
- MEF2 signaling and human diseases.Oncotarget · 2017Review
- Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017Review
- Hypermethylation: Causes and Consequences in Skeletal Muscle Myopathy.Journal of cellular biochemistry · 2017Review
- Expression levels of atherosclerosis-associated miR-143 and miR-145 in the plasma of patients with hyperhomocysteinaemia.BMC cardiovascular disorders · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
An elevated level of homocysteine called hyperhomocysteinemia (HHcy) is associated with pathological cardiac remodeling. Hydrogen sulfide (H2S) acts as a cardioprotective gas; however, the mechanism by which H2S mitigates homocysteine-mediated pathological remodeling in cardiomyocytes is unclear. We hypothesized that H2S ameliorates HHcy-mediated hypertrophy by inducing cardioprotective miR-133a in cardiomyocytes. To test the hypothesis, HL1 cardiomyocytes were treated with (1) plain medium (control, CT), (2) 100 µM of homocysteine (Hcy), (3) Hcy with 30 µM of H2S (Hcy + H2S), and (4) H2S for 24 h. The levels of hypertrophy markers: c-fos, atrial natriuretic peptide (ANP), and beta-myosin heavy chain (β-MHC), miR-133a, and its transcriptional inducer myosin enhancer factor-2C (MEF2C) were determined by Western blotting, RT-qPCR, and immunofluorescence. The activity of MEF2C was assessed by co-immunoprecipitation of MEF2C with histone deacetylase-1(HDAC1). Our results show that H2S ameliorates homocysteine-mediated up-regulation of c-fos, ANP, and β-MHC, and down-regulation of MEF2C and miR-133a. HHcy induces the binding of MEF2C with HDAC1, whereas H2S releases MEF2C from MEF2C-HDAC1 complex causing activation of MEF2C. These findings elicit that HHcy induces cardiac hypertrophy by promoting MEF2C-HDAC1 complex formation that inactivates MEF2C causing suppression of anti-hypertrophy miR-133a in cardiomyocytes. H2S mitigates hypertrophy by inducing miR-133a through activation of MEF2C in HHcy cardiomyocytes. To our knowledge, this is a novel mechanism of H2S-mediated activation of MEF2C and induction of miR-133a and inhibition of hypertrophy in HHcy cardiomyocytes.
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