ReviewCurrent medicinal chemistry2014
Endothelial dysfunction: the link between homocysteine and hydrogen sulfide.
Review in Current medicinal chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
110 citing papers in PubMed, 4 syntheses or guidelines pooled it, 248 citations in OpenAlex.
- Thromboembolic complications of recreational nitrous oxide (ab)use: a systematic review.Journal of thrombosis and thrombolysis · 2022Pooled it
- The association between homocysteine and ischemic stroke subtypes in Chinese: A meta-analysis.Medicine · 2020Pooled it
- Plasma homocysteine concentrations and risk of intracerebral hemorrhage: a systematic review and meta-analysis.Scientific reports · 2018Pooled it
- Homocysteine-lowering interventions for preventing cardiovascular events.The Cochrane database of systematic reviews · 2017Pooled it
- Dose-Dependent Association of Long-Term Metformin Use and Diabetic Nephropathy Risk in Patients with Type 2 Diabetes Mellitus: A Nationwide Population-Based Study in Taiwan.Clinical drug investigation · 2026Article
- Defining metabolic heterogeneity in polyendocrine metabolic ovarian syndrome based on the MTHFR C677T polymorphism: the potential pathway role of homocysteine.Journal of ovarian research · 2026Article
- One-carbon metabolism and cardiovascular disease: Molecular mechanisms, genetic influences, and epigenetic regulation.Biochemistry and biophysics reports · 2026Review
- Predicting late radiation-associated neurocognitive and endocrine toxicity in patients with brain tumors.Journal of neuro-oncology · 2026Article
- Risk of Retinal Vein Occlusion in Patients With Vitamin BJournal of vitreoretinal diseases · 2026Article
- Increased potential for atherogenic changes in asthma: evidence from transcriptomic studies of arterial endothelial cells.Respiratory research · 2026Article
- B vitamins and cardiovascular health: mechanisms, clinical evidence, and precision prevention strategies.Nutrition & metabolism · 2026Review
- Review
- Vascular transcriptional and metabolic changes precede progressive intrarenal microvascular rarefaction in autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2026Article
- Pulmonary thromboembolism and aortic thrombosis due to severe hyperhomocysteinemia with MTHFR C677T mutation: a case report.European heart journal. Case reports · 2026Article
- Association of serum and vitreous homocysteine and uric acid concentrations with post-vitrectomy prognosis in patients with proliferative diabetic retinopathy.World journal of diabetes · 2026Article
- Modulating One-Carbon Metabolism with B-Vitamins to Protect the Retinal Barrier and Prevent Retinal Degeneration.Nutrients · 2026Article
- Sex-Differentiated Threshold Effects of Homocysteine Levels on CKD Risk in Patients with Hypertension and Coronary Artery Disease.Journal of inflammation research · 2026Article
- Homocysteine: Canary in the Coal Mine or Hidden Threat? A Biochemical Study on the Role of Plasma Thiols.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Transsulfuration Pathway Products and HInternational journal of molecular sciences · 2025Review
- Homocysteine Attack on Vascular Endothelium-Old and New Features.International journal of molecular sciences · 2025Review
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
High level of homocysteine (hyperhomocysteinemia, HHcy) is associated with increased risk for vascular disease. Evidence for this emerges from epidemiological studies which show that HHcy is associated with premature peripheral, coronary artery and cerebrovascular disease independent of other risk factors. Possible mechanisms by which homocysteine causes vascular injury include endothelial injury, DNA dysfunction, proliferation of smooth muscle cells, increased oxidative stress, reduced activity of glutathione peroxidase and promoting inflammation. HHcy has been shown to cause direct damage to endothelial cells both in vitro and in vivo. Clinically, this manifests as impaired flow-mediated vasodilation and is mainly due to a reduction in nitric oxide synthesis and bioavailability. The effect of impaired nitric oxide release can in turn trigger and potentiate atherothrombogenesis and oxidative stress. Endothelial damage is a crucial aspect of atherosclerosis and precedes overt manifestation of disease. In addition, endothelial dysfunction is also associated with hypertension, diabetes, ischemia reperfusion injury and neurodegenerative diseases. Homocysteine is a precursor of hydrogen sulfide (H2S) which is formed by transulfuration process catalyzed by the enzymes, cystathionine β-synthase and cystathionine γ-lyase. H2S is a gasotransmitter that has emerged recently as a novel mediator in cardiovascular homeostasis. As a potent vasodilator, it plays several roles which include regulation of vessel diameter, protection of endothelium from redox stress, ischemia reperfusion injury and chronic inflammation. However, the precise mechanism by which it mediates these beneficial effects is complex and still remains unclear. Current evidence indicates H2S modulates cellular functions by a variety of intracellular signaling processes. In this review, we summarize the mechanisms of HHcy-induced endothelial dysfunction and the metabolism and physiological functions of H2S as a protective agent.
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What OpenQuestion holds
Registered trials
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.