Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function.
Endothelial dysfunction is a pathological status of the vascular system, which can be broadly defined as an imbalance between endothelium-dependent vasoconstriction and vasodilation. Endothelial dysfunction is a key event in the progression of many pathological processes including atherosclerosis, type II diabetes and hypertension. Previous reports have demonstrated that pro-inflammatory/immunoeffector cytokines significantly promote endothelial dysfunction while numerous novel anti-inflammatory/immunosuppressive cytokines have recently been identified such as interleukin (IL)-35. However, the effects of anti-inflammatory cytokines on endothelial dysfunction have received much less attention. In this analytical review, we focus on the recent progress attained in characterizing the direct and indirect effects of anti-inflammatory/immunosuppressive cytokines in the inhibition of endothelial dysfunction. Our analyses are not only limited to the importance of endothelial dysfunction in cardiovascular disease progression, but also expand into the molecular mechanisms and pathways underlying the inhibition of endothelial dysfunction by anti-inflammatory/immunosuppressive cytokines. Our review suggests that anti-inflammatory/immunosuppressive cytokines serve as novel therapeutic targets for inhibiting endothelial dysfunction, vascular inflammation and cardio- and cerebro-vascular diseases.
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. yings@temple.edu.
Ying
Y
Shao
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. zjcheng@temple.edu.
Zhongjian
Z
Cheng
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. xinyuan.li@temple.edu.
Xinyuan
X
Li
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. v.chernaya@temple.edu.
Valeria
V
Chernaya
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. hongw@temple.edu.
Hong
H
Wang
Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, MERB 1059, 3500 North Broad Street, Philadelphia, PA, 19140, USA. xfyang@temple.edu.|Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, 19140, USA. xfyang@temple.edu.
Xiao-feng
XF
Yang
D000818:Animals; D016207:Cytokines / Q000276:immunology*; D004730:Endothelium, Vascular / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007108:Immune Tolerance; D007249:Inflammation / Q000276:immunology / Q000473:pathology
D016207:Cytokines