Role of Nitric Oxide and Hydrogen Sulfide in Neuronal and Glial Cell Death in Neurodegenerative Processes

被引:1
|
作者
Rodkin, S. V. [1 ]
Nwosu, C. D. [1 ]
机构
[1] Don State Tech Univ, Fac Bioengn & Vet Med, Dept Bioengn, Rostov Na Donu 344000, Russia
来源
BIOLOGICHESKIE MEMBRANY | 2023年 / 40卷 / 05期
关键词
nitric oxide; hydrogen sulfide; neurodegeneration; neurons; glial cells; oxidative stress; apoptosis; autophagy; axotomy; INDUCED OXIDATIVE STRESS; TRAUMATIC BRAIN-INJURY; MITOCHONDRIAL DYSFUNCTION; AXONAL DEGENERATION; FUNCTIONAL RECOVERY; S-NITROSYLATION; UP-REGULATION; H2S PROTECTS; IN-VITRO; APOPTOSIS;
D O I
10.31857/S0233475523050067
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Neurodegeneration is a complex progressive pathological process leading to the neuronal death, which is induced by various external and internal factors. Neurodegenerative diseases, injuries of the central and peripheral nervous system, mental disorders, and a number of other pathological conditions, accompanied by functional and structural degradation of neurons and their death, is a serious problem in the global healthcare system, as due to these diseases millions of people around the world become disabled or die every year. The situation is complicated by the lack of selective, clinically effective neuroprotective drugs. It has been shown that nitric oxide (NO) and hydrogen sulfide (H2S) are actively involved in neurodegeneration and cell death of neurons and glia, but their role is not completely clear. This review considers NO- and H2S-dependent signaling mechanisms underlying the pathogenesis of neurodegenerative processes. The prospects for further studies of the role of NO and H2S in the nervous tissue under conditions of pathological conditions associated with neurodegeneration are considered.
引用
收藏
页码:306 / 327
页数:22
相关论文
共 50 条
  • [21] Selective Irreversible Inhibition of Neuronal and Inducible Nitric-oxide Synthase in the Combined Presence of Hydrogen Sulfide and Nitric Oxide
    Heine, Christian L.
    Schmidt, Renate
    Geckl, Kerstin
    Schrammel, Astrid
    Gesslbauer, Bernd
    Schmidt, Kurt
    Mayer, Bernd
    Gorren, Antonius C. F.
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2015, 290 (41) : 24932 - 24944
  • [22] Role of nitric oxide in neurodegenerative diseases
    Schulz, JB
    Matthews, RT
    Beal, MF
    CURRENT OPINION IN NEUROLOGY, 1995, 8 (06) : 480 - 486
  • [23] Hydrogen sulfide, then nitric oxide and vasoprotection
    Chappell, Mark C.
    JOURNAL OF HYPERTENSION, 2018, 36 (03) : 493 - 494
  • [24] Nitric oxide, glial cells and neuronal degeneration in parkinsonism
    Hirsch, EC
    Hunot, S
    TRENDS IN PHARMACOLOGICAL SCIENCES, 2000, 21 (05) : 163 - 165
  • [25] Nitric-oxide-induced depolarization of neuronal mitochondria: implications for neuronal cell death
    Solenski, NJ
    Kostecki, VK
    Dovey, S
    Periasamy, A
    MOLECULAR AND CELLULAR NEUROSCIENCE, 2003, 24 (04) : 1151 - 1169
  • [26] Nitric oxide induction of neuronal endonuclease activity in programmed cell death
    Vincent, AM
    Maiese, K
    EXPERIMENTAL CELL RESEARCH, 1999, 246 (02) : 290 - 300
  • [27] Neuronal cell death and apoptosis in neurodegenerative diseases
    Klockgether, T
    Wüllmer, U
    PARKINSON'S DISEASE, 2002, 1 : 81 - 87
  • [28] Role of nitric oxide and cyclic GMP in glutamate-induced neuronal death
    Carmina Montoliu
    Marta Llansola
    Pilar Monfort
    Regina Corbalan
    Iñigo Fernandez-Marticorena
    Mari -Luz Hernandez-Viadel
    Vicente Felipo
    Neurotoxicity Research, 2001, 3 : 179 - 188
  • [29] Hydrogen sulfide and nitric oxide interactions in inflammation
    Lo Faro, Maria Letizia
    Fox, Bridget
    Whatmore, Jacqueline L.
    Winyard, Paul G.
    Whiteman, Matthew
    NITRIC OXIDE-BIOLOGY AND CHEMISTRY, 2014, 41 : 38 - 47
  • [30] Role of nitric oxide and cyclic GMP in glutamate-induced neuronal death
    Montoliu, Carmina
    Llansola, Marta
    Monfort, Pilar
    Corbalan, Regina
    Fernandez-Marticorena, Inigo
    Hernandez-Viadel, Mari-Luz
    Felipo, Vicente
    NEUROTOXICITY RESEARCH, 2001, 3 (02) : 179 - 188