title: Lower Hydrogen Sulfide Is Associated with Cardiovascular Mortality, Which Involves cPKCβII/Akt Pathway in Chronic Hemodialysis Patients.
abstract: OBJECTIVE
  To evaluate the relationship between plasma hydrogen sulfide (H₂S) and cardiovascular risk markers, including pulse pressure (PP), left ventricular mass index (LVMI) and intima-media thickness (IMT), and mortality in chronic hemodialysis (CHD) patients and further investigate the underlying cardiovascular protection mechanism of H₂S.
  
  
  METHODS
  CHD patients, 113 of them, were studied. Plasma H₂S was measured through zinc acetate reaction. cPKCβII membrane translocation and phosphorylation of Akt were detected by western blot.
  
  
  RESULTS
  Lower plasma H₂S level in CHD patients was predictor of an increased PP, LVMI and IMT. Patients with lower H₂S had a lower survival at the end of the study. H₂S was an independent predictor of all-cause and cardiovascular mortality when adjusted for other risk factors. CHD patients with lower H₂S showed an increase of cPKCβII activation, but phosphorylation of Akt decreased. The level of VCAM-1 and ICAM-1 increased significantly.
  
  
  CONCLUSIONS
  Lower plasma H₂S in CHD patients is associated with cardiovascular risk factors and mortality, which may be mediated by the cPKCβII/Akt pathway and further VCAM-1/ICAM-1 upregulation.
authors.affiliation: Department of Blood Purification, Beijing Chao-Yang Hospital, Capital Medical University, Nephrology Faculty, Capital Medical University, Beijing, China.
authors.forename: Su-Juan
authors.initials: SJ
authors.lastname: Feng
authors.forename: Han
authors.initials: H
authors.lastname: Li
authors.forename: Shi-Xiang
authors.initials: SX
authors.lastname: Wang
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood* / Q000150:complications / Q000401:mortality / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology; D059168:Carotid Intima-Media Thickness; D005260:Female; D005786:Gene Expression Regulation; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006862:Hydrogen Sulfide / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000235:genetics; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000401:mortality / Q000628:therapy; D007963:Leukocytes, Mononuclear / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010766:Phosphorylation; D011379:Prognosis; D064546:Protein Kinase C beta / Q000097:blood* / Q000235:genetics; D051057:Proto-Oncogene Proteins c-akt / Q000097:blood* / Q000235:genetics; D006435:Renal Dialysis; D015398:Signal Transduction; D016019:Survival Analysis; D014511:Uremia / Q000097:blood* / Q000150:complications / Q000401:mortality / Q000628:therapy; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood / Q000235:genetics
chemical_list: D015415:Biomarkers; C573420:ICAM1 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D051057:Proto-Oncogene Proteins c-akt; D064546:Protein Kinase C beta; D006862:Hydrogen Sulfide