Role of Nitric Oxide and Protein S-Nitrosylation in Ischemia-Reperfusion Injury

被引：16

作者：

Lee, Hyang-Mi ^{[1
]}

Choi, Ji Woong ^{[2
]}

Choi, Min Sik ^{[3
]}

机构：

[1] Dongduk Womens Univ, Coll Pharm, Seoul 02748, South Korea

[2] Gachon Univ, Coll Pharm, Incheon 21936, South Korea

[3] Dongduk Womens Univ, Coll Pharm, Lab Pharmacol, Seoul 02748, South Korea

来源：

ANTIOXIDANTS | 2022年 / 11卷 / 01期

基金：

新加坡国家研究基金会;

关键词：

ischemia-reperfusion injury; nitric oxide; protein S-nitrosylation; ADHESION MOLECULE EXPRESSION; DECREASES INFARCTION SIZE; REGULATING KINASE 1; MYOCARDIAL-ISCHEMIA; LIVER ISCHEMIA; KAPPA-B; ENDOTHELIAL DYSFUNCTION; L-ARGININE; NEUTROPHIL INFILTRATION; SODIUM-NITROPRUSSIDE;

D O I：

10.3390/antiox11010057

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Ischemia-reperfusion injury (IRI) is a process in which damage is induced in hypoxic tissue when oxygen supply is resumed after ischemia. During IRI, restoration of reduced nitric oxide (NO) levels may alleviate reperfusion injury in ischemic organs. The protective mechanism of NO is due to anti-inflammatory effects, antioxidant effects, and the regulation of cell signaling pathways. On the other hand, it is generally known that S-nitrosylation (SNO) mediates the detrimental or protective effect of NO depending on the action of the nitrosylated target protein, and this is also applied in the IRI process. In this review, the effect of each change of NO and SNO during the IRI process was investigated.

引用

页数：14

共 119 条

[51] NITRIC-OXIDE PRODUCTION DURING FOCAL CEREBRAL-ISCHEMIA IN RATS [J].

KADER, A ;

FRAZZINI, VI ;

SOLOMON, RA ;

TRIFFILETTI, RR .

STROKE, 1993, 24 (11) :1709-1716

[52] Neuronal expression of the mitochondrial protein prohibitin confers profound neuroprotection in a mouse model of focal cerebral ischemia [J].

Kahl, Anja ;

Anderson, Corey J. ;

Qian, Liping ;

Voss, Henning ;

Manfredi, Giovanni ;

Iadecola, Costantino ;

Zhou, Ping .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2018, 38 (06) :1010-1020

[53] ISCHEMIA REPERFUSION INJURY - A REVIEW [J].

KERRIGAN, CL ;

STOTLAND, MA .

MICROSURGERY, 1993, 14 (03) :165-175

[54] Tackling endothelial dysfunction by modulating NOS uncoupling: new insights into its pathogenesis and therapeutic possibilities [J].

Kietadisorn, Rinrada ;

Juni, Rio P. ;

Moens, An L. .

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2012, 302 (05) :E481-E495

[55] The effect of nitric oxide on ischemia-reperfusion injury in rat liver [J].

Köken, T ;

Inal, M .

CLINICA CHIMICA ACTA, 1999, 288 (1-2) :55-62

[56] GAPDH mediates nitrosylation of nuclear proteins [J].

Kornberg, Michael D. ;

Sen, Nilkantha ;

Hara, Makoto R. ;

Juluri, Krishna R. ;

Nguyen, Judy Van K. ;

Snowman, Adele M. ;

Law, Lindsey ;

Hester, Lynda D. ;

Snyder, Solomon H. .

NATURE CELL BIOLOGY, 2010, 12 (11) :1094-U89

[57]

Kuroki K, 2004, HEPATO-GASTROENTEROL, V51, P1404

[58] The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia-reperfusion [J].

Lefer, AM ;

Lefer, DJ .

CARDIOVASCULAR RESEARCH, 1996, 32 (04) :743-751

[59] Endogenous S-nitrosothiols protect against myocardial injury [J].

Lima, Brian ;

Lam, Gregory K. W. ;

Xie, Liang ;

Diesen, Diana L. ;

Villamizar, Nestor ;

Nienaber, Jeffrey ;

Messina, Emily ;

Bowles, Dawn ;

Kontos, Christopher D. ;

Hare, Joshua M. ;

Stamler, Jonathan S. ;

Rockman, Howard A. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (15) :6297-6302

[60] A REDOX-BASED MECHANISM FOR THE NEUROPROTECTIVE AND NEURODESTRUCTIVE EFFECTS OF NITRIC-OXIDE AND RELATED NITROSO-COMPOUNDS [J].

LIPTON, SA ;

CHOI, YB ;

PAN, ZH ;

LEI, SZZ ;

CHEN, HSV ;

SUCHER, NJ ;

LOSCALZO, J ;

SINGEL, DJ ;

STAMLER, JS .

NATURE, 1993, 364 (6438) :626-632

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