ArticlePloS one2015
Homocysteine Induces Collagen I Expression by Downregulating Histone Methyltransferase G9a.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Dysregulated homocysteine metabolism and cardiovascular disease and clinical treatments.Molecular and cellular biochemistry · 2025Review
- Post-translational modifications of collagen and its related diseases in metabolic pathways.Acta pharmaceutica Sinica. B · 2025Review
- The histone H3K9 methyltransferase G9a regulates tendon formation during development.Scientific reports · 2024Article
- Non-Conventional Risk Factors: "Fact" or "Fake" in Cardiovascular Disease Prevention?Biomedicines · 2023Review
- IOX1 protects from TGF-β induced fibrosis in LX-2 cells via the regulation of extracellular matrix protein expression.Experimental and therapeutic medicine · 2021Article
- EZH2-inhibitor DZNep enhances apoptosis of renal tubular epithelial cells in presence and absence of cisplatin.Cell division · 2020Article
- CERA Attenuates Kidney Fibrogenesis in the db/db Mouse by Influencing the Renal Myofibroblast Generation.Journal of clinical medicine · 2018Article
- Hypermethylation: Causes and Consequences in Skeletal Muscle Myopathy.Journal of cellular biochemistry · 2017Review
- Cochlear Homocysteine Metabolism at the Crossroad of Nutrition and Sensorineural Hearing Loss.Frontiers in molecular neuroscience · 2017Review
- Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.International journal of biological sciences · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperhomocysteinemia (HHcy) leads to several clinical manifestations including hepatic fibrosis. Excess deposition of extracellular matrix (ECM) components including collagen is the eponymous lesion of liver fibrosis. In this study, we demonstrated that elevated concentration of Hcy induced the expression of collagen type I in cultured human liver cells as well as in liver tissue of HHcy mice. Meanwhile, Hcy inhibited the expression of histone methyltransferase G9a. Mechanistically, silencing endogenous G9a by siRNA enhanced the promoter activity of COL1A1 in LO2 cells. Conversely, overexpressing G9a inhibited the promoter activity of COL1A1. CHIP assay demonstrated that G9a binds to the neuron-restrictive silencer element (NRSE) on the promoter of COL1A1. Hcy treatment decreased the binding of G9a on NRSE, which in turn decreased the level of H3K9me2 on the promoter of COL1A1, led to upregulation of COL1A1. Taken together, these results provide a novel mechanism on explaining how HHcy promotes ECM production.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.