ArticleInternational journal of molecular sciences2015
Homocysteine Triggers Inflammatory Responses in Macrophages through Inhibiting CSE-H2S Signaling via DNA Hypermethylation of CSE Promoter.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- Association of homocysteine with ankylosing spondylitis: a systematic review and meta-analysis.Advances in rheumatology (London, England) · 2021Pooled it
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- Comparative Effects of Heart Failure Medications on Cardiac Remodeling via the Hydrogen Sulfide (HDiseases (Basel, Switzerland) · 2026Review
- TNF-α/PAD4 axis drives hyperhomocysteine-induced white matter injury after acute ischemic stroke.Acta pharmacologica Sinica · 2026Article
- A Paradigm Shift of HCurrent issues in molecular biology · 2026Review
- Evaluation of Alkaline-Labile Sulfane Sulfur in Biological Samples: The Influence of Hyperhomocysteinemia and Oxidative Stress.Biomolecules · 2026Article
- Role and Relationship Between Homocysteine and HMolecular neurobiology · 2025Review
- The Role of Micronutrients in Atherosclerosis: Mechanisms and Clinical Application.Journal of cellular and molecular medicine · 2025Review
- The Role of Purinergic Mechanisms in the Excitability of Trigeminal Afferents of Rats with Prenatal Hyperhomocysteinemia.Biomolecules · 2025Article
- Vascular inflammation in chronic kidney disease: the role of uremic toxins in macrophage activation.Frontiers in cardiovascular medicine · 2025Review
- Article
- Influence of Coronary Artery Bypass Grafts on Blood Aminothiols in Patients with Coronary Artery Disease.Metabolites · 2023Article
- From Gasotransmitter to Immunomodulator: The Emerging Role of Hydrogen Sulfide in Macrophage Biology.Antioxidants (Basel, Switzerland) · 2023Review
- The Roles of Aerobic Exercise and Folate Supplementation in Hyperhomocysteinemia-Accelerated Atherosclerosis.Acta Cardiologica Sinica · 2023Article
- Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Resolving Geroplasticity to the Balance of Rejuvenins and Geriatrins.Aging and disease · 2022Article
- The Role of Hydrogen Sulfide in Plaque Stability.Antioxidants (Basel, Switzerland) · 2022Review
- Serum Homocysteine and Vascular Calcification: Advances in Mechanisms, Related Diseases, and Nutrition.Korean journal of family medicine · 2022Article
- Diallyl Trisulfide Promotes Placental Angiogenesis by Regulating Lipid Metabolism and Alleviating Inflammatory Responses in Obese Pregnant Mice.Nutrients · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperhomocysteinemia (HHcy) is an independent risk factor of atherosclerosis and other cardiovascular diseases. Unfortunately, Hcy-lowering strategies were found to have limited effects in reducing cardiovascular events. The underlying mechanisms remain unclear. Increasing evidence reveals a role of inflammation in the pathogenesis of HHcy. Homocysteine (Hcy) is a precursor of hydrogen sulfide (H2S), which is formed via the transsulfuration pathway catalyzed by cystathionine β-synthase and cystathionine γ-lyase (CSE) and serves as a novel modulator of inflammation. In the present study, we showed that methionine supplementation induced mild HHcy in mice, associated with the elevations of TNF-α and IL-1β in the plasma and reductions of plasma H2S level and CSE expression in the peritoneal macrophages. H2S-releasing compound GYY4137 attenuated the increases of TNF-α and IL-1β in the plasma of HHcy mice and Hcy-treated raw264.7 cells while CSE inhibitor PAG exacerbated it. Moreover, the in vitro study showed that Hcy inhibited CSE expression and H2S production in macrophages, accompanied by the increases of DNA methyltransferase (DNMT) expression and DNA hypermethylation in cse promoter region. DNMT inhibition or knockdown reversed the decrease of CSE transcription induced by Hcy in macrophages. In sum, our findings demonstrate that Hcy may trigger inflammation through inhibiting CSE-H2S signaling, associated with increased promoter DNA methylation and transcriptional repression of cse in macrophages.
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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.