title: Interactions of hyperhomocysteinemia and T cell immunity in causation of hypertension.
abstract: Although hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular diseases (CVD), there is a debate on whether HHcy is a risk factor or just a biomarker. Interestingly, homocysteine lowering strategies in humans had very little effect on reducing the cardiovascular risk, as compared with animals; this may suggest heterogeneity in human population and epigenetic alterations. Moreover, there are only few studies that suggest the idea that HHcy contributes to CVD in the presence of other risk factors such as inflammation, a known risk factor for CVD. Elevated levels of homocysteine have been shown to contribute to inflammation. Here, we highlight possible relationships between homocysteine, T cell immunity, and hypertension, and summarize the evidence that suggested these factors act together in increasing the risk for CVD. In light of this new evidence, we further propose that there is a need for evaluation of the causes of HHcy, defective remethylation or defective transsulfuration, which may differentially modulate hypertension progression, not just the homocysteine levels.
authors.affiliation: Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.|Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
authors.forename: Sudhakar
authors.initials: S
authors.lastname: Veeranki
authors.affiliation: Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.|Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
authors.forename: Siva K
authors.initials: SK
authors.lastname: Gandhapudi
authors.affiliation: Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.|Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
authors.forename: Suresh C
authors.initials: SC
authors.lastname: Tyagi
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000150:complications* / Q000276:immunology; D006973:Hypertension / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D007111:Immunity, Cellular; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology; D008213:Lymphocyte Activation; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D006710:Homocysteine
keywords: T cells; cardiovascular disease; hyperhomocysteinemia; hyperhomocystéinémie; hypertension; inflammation; lymphocytes T; maladie cardiovasculaire