The Relationship Between Protein S-Nitrosylation and Human Diseases: A Review

被引:31
作者
Zhang, Yadi [1 ,2 ]
Deng, Yuzhen [1 ,2 ]
Yang, Xiaoxi [1 ,2 ]
Xue, Hongmei [1 ,2 ]
Lang, Yumiao [1 ,2 ]
机构
[1] Hebei Univ, Coll Publ Hlth, Key Lab Publ Hlth Safety Hebei Prov, 180 Wusidong Rd, Baoding 071002, Peoples R China
[2] Hebei Univ, Inst Life Sci & Green Dev, Key Lab Med Chem & Mol Diag, Minist Educ, Baoding 071002, Peoples R China
基金
中国国家自然科学基金;
关键词
Nitric oxide; S-nitrosylation; Denitrosylation; Human diseases; Mechanism; NITRIC-OXIDE SYNTHASE; PARKINSONS-DISEASE; E-CADHERIN; MUSCULAR-DYSTROPHY; ALZHEIMERS-DISEASE; ALPHA-CATENIN; KINASE-II; THIOREDOXIN; DYSFUNCTION; BETA;
D O I
10.1007/s11064-020-03136-6
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
S-nitrosylation (SNO) is a covalent post-translational oxidative modification. The reaction is the nitroso group (-NO) to a reactive cysteine thiol within a protein to form the SNO. In recent years, a variety of proteins in human body have been found to undergo thiol nitrosylation under specific conditions. Protein SNO, which is closely related to cardiovascular disease, Parkinson's syndrome, Alzheimer's disease and tumors, plays an important role in regulatory mechanism of protein function in both physiological and pathological pathways, such as in cellular homeostasis and metabolism. This review discusses possible molecular mechanisms protein SNO modification, such as the role of NO in vivo and the formation mechanism of SNO, with particular emphasis on mechanisms utilized by SNO to cause certain diseases of human. Importantly, the effect of SNO on diseases is multifaceted and multi-channel, and its critical value in vivo is not well defined. Intracellular redox environment is also a key factor affecting its level. Therefore, we should pay more attention to the equilibrium relationship between SNO and denitrosylation pathway in the future researches. These findings provide theoretical support for the improvement or treatment of diseases from the point of view of SNO.
引用
收藏
页码:2815 / 2827
页数:13
相关论文
共 96 条
[1]   Loss of α-Catenin Decreases the Strength of Single E-cadherin Bonds between Human Cancer Cells [J].
Bajpai, Saumendra ;
Feng, Yunfeng ;
Krishnamurthy, Ranjini ;
Longmore, Gregory D. ;
Wirtz, Denis .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (27) :18252-18259
[2]   Identifying Functional Cysteine Residues in the Mitochondria [J].
Bak, Daniel W. ;
Pizzagalli, Mattia D. ;
Weerapana, Eranthie .
ACS CHEMICAL BIOLOGY, 2017, 12 (04) :947-957
[3]   Altered S-nitrosylation of p53 is responsible for impaired antioxidant response in skeletal muscle during aging [J].
Baldelli, Sara ;
Ciriolo, Maria Rosa .
AGING-US, 2016, 8 (12) :3450-+
[4]   Nitric Oxide Synthase-2-Derived Nitric Oxide Drives Multiple Pathways of Breast Cancer Progression [J].
Basudhar, Debashree ;
Somasundaram, Veena ;
de Oliveira, Graciele Almeida ;
Kesarwala, Aparna ;
Heinecke, Julie L. ;
Cheng, Robert Y. ;
Glynn, Sharon A. ;
Ambs, Stefan ;
Wink, David A. ;
Ridnour, Lisa A. .
ANTIOXIDANTS & REDOX SIGNALING, 2017, 26 (18) :1044-1058
[5]   Protein denitrosylation: enzymatic mechanisms and cellular functions [J].
Benhar, Moran ;
Forrester, Michael T. ;
Stamler, Jonathan S. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2009, 10 (10) :721-732
[6]   α-Synuclein Regulates Iron Homeostasis via Preventing Parkin-Mediated DMT1 Ubiquitylation in Parkinson's Disease Models [J].
Bi, Mingxia ;
Du, Xixun ;
Jiao, Qian ;
Liu, Zhiguo ;
Jiang, Hong .
ACS CHEMICAL NEUROSCIENCE, 2020, 11 (11) :1682-1691
[7]   Healthspan Maintenance and Prevention of Parkinson's-like Phenotypes with Hydroxytyrosol and Oleuropein Aglycone in C. elegans [J].
Brunetti, Giovanni ;
Di Rosa, Gabriele ;
Scuto, Maria ;
Leri, Manuela ;
Stefani, Massimo ;
Schmitz-Linneweber, Christian ;
Calabrese, Vittorio ;
Saul, Nadine .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2020, 21 (07)
[8]   Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications [J].
Bubber, P ;
Haroutunian, V ;
Fisch, G ;
Blass, JP ;
Gibson, GE .
ANNALS OF NEUROLOGY, 2005, 57 (05) :695-703
[9]  
Bukholm IK, 1998, J PATHOL, V185, P262, DOI 10.1002/(SICI)1096-9896(199807)185:3<262::AID-PATH97>3.0.CO
[10]  
2-Y