ArticleIndian journal of clinical biochemistry : IJCB2000
Hyperhomocysteinemia and cardiovascular disease: The nutritional perspectives.
Article in Indian journal of clinical biochemistry : IJCB, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Effect of nitroso-redox imbalance on male reproduction.Translational andrology and urology · 2018Review
- Folic acid ameliorates celecoxib cardiotoxicity in a doxorubicin heart failure rat model.Pharmaceutical biology · 2017Article
- Novel study on N-nitrosamines as risk factors of cardiovascular diseases.BioMed research international · 2014Article
- Oxidative/Nitrosative stress and the pathobiology of chronic obstructive pulmonary disease.Journal of clinical and diagnostic research : JCDR · 2013Article
- Polymorphism (C677T) in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene: A preliminary study on north Indian men.Indian journal of clinical biochemistry : IJCB · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several members of the vitamin B-complex family are known to participate in the normal metabolism of homocysteine (Hcy). Leaving aside the genetic determinants of hyperhomocysteinemia (HHC), the deficiencies of these vitamins can also result in HHC. The situation of sustained and long standing HHC is likely to be prevalent in population groups with low/average socio-economic status, geriatric population and alcohol abusers. If not corrected by supplementation, these population groups certainly are more vulnerable to develop atherosclerosis (AS) and subsequently, cardiovascular disease (CVD). Hyperhomocysteinemia per se and/or HHC-induced oxidative stress result(s) in chronic chemical endothelial injury/dysfunction, smooth muscle proliferation, prothrombotic state and oxidation of low density lipoproteins (LDL) leading to diverse cardiovascular complications. In the first decade of the new millennium, major research efforts would be directed towards understanding the basic mechanism of HHC-induced oxidative stress and the pathophysiology of HHC-induced CVD, culminating in the evolution of hitherto unknown therapeutic strategies such as nutriceuticals and oxidant-antidotes.
Indexed as
Identifiers
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.