Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.
Homocysteine (Hcy) is a sulfur-containing amino acid, which forms as an intermediate during methionine metabolism. High levels of plasma Hcy, also known as hyperhomocysteinemia (HHcy), are always associated with kidney insufficiency [4,5,26,31]. Results from recent studies have indicated that HHcy downregulates hydrogen sulfide (H2S) level and reduces endothelial nitric oxide synthase (eNOS) [18,22]. In addition, through imbalance of matrix metalloproteinases (MMP) and tissue inhibitor of metalloproteinases (TIMP), Hcy accumulates extracellular matrix (ECM) protein in the glomerulo-tubulointerstitial space [21,23,24]. These contribute to renovascular remodeling including renal fibrosis and dysfunction. Although Hcy is known for independent vascular risk factor, the mechanism of renal fibrosis in HHcy is largely unknown. In the tissue, Hcy however metabolizes by three endogenous enzymes: cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST) to produce H2S, a gaseous molecule of tremendous biological importance. This editorial highlights some of the recent updates and future directions of renoprotection by H2S in HHcy.
Sen U (2011) Renoprotection by hydrogen sulfide in hyperhomocysteinemia. Anatom Physiol 1:e111.
https://www.omicsonline.org/renoprotection-by-hydrogen-sulfide-in-hyperhomocysteinemia-2161-0940.1000e111.php?aid=3369
Spanish 
Chinese 
Russian 
German 
French 
Japanese 
Portuguese 
Hindi