PMID- 27398734 OWN - NLM STAT- MEDLINE DCOM- 20170321 LR - 20181113 IS - 1205-7541 (Electronic) IS - 0008-4212 (Print) IS - 0008-4212 (Linking) VI - 95 IP - 3 DP - 2017 Mar TI - Interactions of hyperhomocysteinemia and T cell immunity in causation of hypertension. PG - 239-246 LID - 10.1139/cjpp-2015-0568 [doi] AB - 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. FAU - Veeranki, Sudhakar AU - Veeranki S AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. FAU - Gandhapudi, Siva K AU - Gandhapudi SK AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. FAU - Tyagi, Suresh C AU - Tyagi SC AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. AD - Department of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA. LA - eng GR - R01 DK104653/DK/NIDDK NIH HHS/United States GR - R01 HL074185/HL/NHLBI NIH HHS/United States GR - R01 HL108621/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Review DEP - 20160428 PL - Canada TA - Can J Physiol Pharmacol JT - Canadian journal of physiology and pharmacology JID - 0372712 RN - 0 (Biomarkers) RN - 0 (Inflammation Mediators) RN - 0LVT1QZ0BA (Homocysteine) SB - IM MH - Animals MH - Biomarkers/blood MH - *Blood Pressure MH - Homocysteine/*blood MH - Humans MH - Hyperhomocysteinemia/blood/*complications/immunology MH - Hypertension/blood/*etiology/immunology/physiopathology MH - *Immunity, Cellular MH - Inflammation Mediators/blood/immunology MH - Lymphocyte Activation MH - Prognosis MH - Risk Assessment MH - Risk Factors MH - Signal Transduction MH - T-Lymphocytes/*immunology/metabolism MH - Up-Regulation PMC - PMC5519337 MID - NIHMS877137 OTO - NOTNLM OT - T cells OT - cardiovascular disease OT - hyperhomocysteinemia OT - hyperhomocysteinemie OT - hypertension OT - inflammation OT - lymphocytes T OT - maladie cardiovasculaire EDAT- 2016/07/12 06:00 MHDA- 2017/03/23 06:00 PMCR- 2017/07/20 CRDT- 2016/07/12 06:00 PHST- 2016/07/12 06:00 [pubmed] PHST- 2017/03/23 06:00 [medline] PHST- 2016/07/12 06:00 [entrez] PHST- 2017/07/20 00:00 [pmc-release] AID - 10.1139/cjpp-2015-0568 [doi] PST - ppublish SO - Can J Physiol Pharmacol. 2017 Mar;95(3):239-246. doi: 10.1139/cjpp-2015-0568. Epub 2016 Apr 28.