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A cardioprotective insight of the cystathionine γ-lyase/hydrogen sulfide pathway.
Int J Cardiol Heart Vasc. 2015 Jun 01; 7:51-57.IJ

Abstract

Traditionally, hydrogen sulfide (H2S) was simply considered as a toxic and foul smelling gas, but recently H2S been brought into the spot light of cardiovascular research and development. Since the 1990s, H2S has been mounting evidence of physiological properties such as immune modification, vascular relaxation, attenuation of oxidative stress, inflammatory mitigation, and angiogenesis. H2S has since been recognized as the third physiological gaseous signaling molecule, along with CO and NO [65,66]. H2S is produced endogenously through several key enzymes, including cystathionine β-lyase (CBE), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (MST)/cysteine aminotransferase (CAT). These specific enzymes are expressed accordingly in various organ systems and CSE is the predominant H2S-producing enzyme in the cardiovascular system. The cystathionine γ-lyase (CSE)/H2S pathway has demonstrated various cardioprotective effects, including anti-atherosclerosis, anti-hypertension, pro-angiogenesis, and attenuation of myocardial ischemia-reperfusion injury. CSE exhibits its anti-atherosclerotic effect through 3 mechanisms, namely reduction of chemotactic factor inter cellular adhesion molecule-1 (ICAM-1) and CX3CR1, inhibition of macrophage lipid uptake, and induction of smooth muscle cell apoptosis via MAPK pathway. The CSE/H2S pathway's anti-hypertensive properties are demonstrated via aortic vasodilation through several mechanisms, including the direct stimulation of KATP channels of vascular smooth muscle cells (VSMCs), induction of MAPK pathway, and reduction of homocysteine buildup. Also, CSE/H2S pathway plays an important role in angiogenesis, particularly in increased endothelial cell growth and migration, and in increased vascular network length. In myocardial ischemia-reperfusion injuries, CSE/H2S pathway has shown a clear cardioprotective effect by preserving mitochondria function, increasing antioxidant production, and decreasing infarction injury size. However, CSE/H2S pathway's role in inflammation mitigation is still clouded, due to both pro and anti-inflammatory results presented in the literature, depending on the concentration and form of H2S used in specific experiment models.

Authors+Show Affiliations

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Departments of Physiology and Medicine/CVRL, UCLA School of Medicine, Los Angeles, CA 90095, USA.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28785645

Citation

Huang, Steve, et al. "A Cardioprotective Insight of the Cystathionine Γ-lyase/hydrogen Sulfide Pathway." International Journal of Cardiology. Heart & Vasculature, vol. 7, 2015, pp. 51-57.
Huang S, Li H, Ge J. A cardioprotective insight of the cystathionine γ-lyase/hydrogen sulfide pathway. Int J Cardiol Heart Vasc. 2015;7:51-57.
Huang, S., Li, H., & Ge, J. (2015). A cardioprotective insight of the cystathionine γ-lyase/hydrogen sulfide pathway. International Journal of Cardiology. Heart & Vasculature, 7, 51-57. https://doi.org/10.1016/j.ijcha.2015.01.010
Huang S, Li H, Ge J. A Cardioprotective Insight of the Cystathionine Γ-lyase/hydrogen Sulfide Pathway. Int J Cardiol Heart Vasc. 2015 Jun 1;7:51-57. PubMed PMID: 28785645.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A cardioprotective insight of the cystathionine γ-lyase/hydrogen sulfide pathway. AU - Huang,Steve, AU - Li,Hua, AU - Ge,Junbo, Y1 - 2015/02/07/ PY - 2014/08/02/received PY - 2014/11/29/revised PY - 2015/01/20/accepted PY - 2017/8/9/entrez PY - 2015/2/7/pubmed PY - 2015/2/7/medline KW - Akt, protein kinase B KW - Angiogenesis KW - Atherosclerosis KW - BCA, brachiocephalic artery KW - CAM, chorioallantoic membrane KW - CAT, cysteine aminotransferase KW - CBS, cystathionine β-lyase KW - CLP, cecal ligation and puncture KW - CSE KO, CSE knock out KW - CSE, cystathionine γ-lyase KW - CTO, chronic total occlusion KW - CX3CL1, chemokine (C-X3-C Motif) ligand 1 KW - CX3CR1, CX3C chemokine receptor 1 KW - Cystathionine γ-lyase KW - EC, endothelial cell KW - ERK, extracellular signal-regulated kinase KW - GAPDH, glyceraldehyde 3-phosphate dehydrogenase KW - GSH-Px, glutathione peroxidase KW - GYY4137, morpholin-4-Ium-4-methoxyphenyl(morpholino) phosphinodithioate KW - H2S, hydrogen sulfide KW - HUVECs, human umbilical vein endothelial cells KW - Hydrogen sulfide KW - ICAM-1, inter cellular adhesion molecule-1 KW - IMT, intima–media complex thickness KW - Ischemia–reperfusion injury KW - LPS, lipopolysaccharide KW - MAPK, mitogen-activated protein kinase KW - MPO, myeloperoxidase KW - MST, 3-mercaptopyruvate sulfurtransferase KW - NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells KW - Nrf2, nuclear factor erythroid 2-related factor 2 KW - PAG, DL-propagylglycine KW - PPAR-γ, peroxisome proliferator-activated receptor KW - PTPN1, protein tyrosine phosphatase, non-receptor type 1 KW - ROS, reactive oxygen species KW - S-diclofenac, 2-[(2,6-dichlorophenyl)amino]benzeneacetic acid 4-(3H-1,2-dithiole-3-thione-5-Yl)-phenyl ester KW - SAH, S-adenosylhomocysteine KW - SAM, S-adenosylmethionine KW - SMCs, smooth muscle cells KW - SOD, superoxide dismutase KW - VEGF, vascular endothelial growth factor KW - VSMCs, vascular smooth muscle cells KW - Vasorelaxation KW - l-NAME, NG-nitro-l-arginine methyl ester KW - oxLDL, oxidized low density lipoprotein SP - 51 EP - 57 JF - International journal of cardiology. Heart & vasculature JO - Int J Cardiol Heart Vasc VL - 7 N2 - Traditionally, hydrogen sulfide (H2S) was simply considered as a toxic and foul smelling gas, but recently H2S been brought into the spot light of cardiovascular research and development. Since the 1990s, H2S has been mounting evidence of physiological properties such as immune modification, vascular relaxation, attenuation of oxidative stress, inflammatory mitigation, and angiogenesis. H2S has since been recognized as the third physiological gaseous signaling molecule, along with CO and NO [65,66]. H2S is produced endogenously through several key enzymes, including cystathionine β-lyase (CBE), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (MST)/cysteine aminotransferase (CAT). These specific enzymes are expressed accordingly in various organ systems and CSE is the predominant H2S-producing enzyme in the cardiovascular system. The cystathionine γ-lyase (CSE)/H2S pathway has demonstrated various cardioprotective effects, including anti-atherosclerosis, anti-hypertension, pro-angiogenesis, and attenuation of myocardial ischemia-reperfusion injury. CSE exhibits its anti-atherosclerotic effect through 3 mechanisms, namely reduction of chemotactic factor inter cellular adhesion molecule-1 (ICAM-1) and CX3CR1, inhibition of macrophage lipid uptake, and induction of smooth muscle cell apoptosis via MAPK pathway. The CSE/H2S pathway's anti-hypertensive properties are demonstrated via aortic vasodilation through several mechanisms, including the direct stimulation of KATP channels of vascular smooth muscle cells (VSMCs), induction of MAPK pathway, and reduction of homocysteine buildup. Also, CSE/H2S pathway plays an important role in angiogenesis, particularly in increased endothelial cell growth and migration, and in increased vascular network length. In myocardial ischemia-reperfusion injuries, CSE/H2S pathway has shown a clear cardioprotective effect by preserving mitochondria function, increasing antioxidant production, and decreasing infarction injury size. However, CSE/H2S pathway's role in inflammation mitigation is still clouded, due to both pro and anti-inflammatory results presented in the literature, depending on the concentration and form of H2S used in specific experiment models. SN - 2352-9067 UR - https://www.unboundmedicine.com/medline/citation/28785645/A_cardioprotective_insight_of_the_cystathionine_γ_lyase/hydrogen_sulfide_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S2352-9067(15)00011-1 DB - PRIME DP - Unbound Medicine ER -
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