Mitochondrial dysfunction and inflammasome activation in neurodegenerative diseases: Mechanisms and therapeutic implications

被引:8
作者
Hamzeh, Olia [1 ,2 ,3 ]
Rabiei, Fatemeh [1 ]
Shakeri, Mahdi [1 ]
Parsian, Hadi [2 ,3 ]
Saadat, Payam [4 ]
Rostami-Mansoor, Sahar [2 ,3 ]
机构
[1] Babol Univ Med Sci, Student Res Comm, Babol, Iran
[2] Babol Univ Med Sci, Hlth Res Inst, Cellular & Mol Biol Res Ctr, Babol, Iran
[3] Babol Univ Med Sci, Fac Med, Dept Clin Biochem, Babol, Iran
[4] Babol Univ Med Sci, Hlth Res Inst, Mobil Impairment Res Ctr, Babol, Iran
关键词
Mitochondrial dysfunction; Inflammasome; NLRP3; Neurodegenerative disease; AMYOTROPHIC-LATERAL-SCLEROSIS; NLRP3; INFLAMMASOME; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; MULTIPLE-SCLEROSIS; KAPPA-B; COGNITIVE IMPAIRMENT; SUPEROXIDE-DISMUTASE; ENERGY-METABOLISM; OXIDATIVE DAMAGE;
D O I
10.1016/j.mito.2023.10.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Impaired mitochondrial function is crucial to the pathogenesis of several neurodegenerative diseases. It causes the release of mitochondrial DNA (mtDNA), mitochondrial reactive oxygen species (mtROS), ATP, and cardiolipin, which activate the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome. NLRP3 inflammasome is an important innate immune system element contributing to neuroinflammation and neurodegeneration. Therefore, targeting the NLRP3 inflammasome has become an interesting therapeutic approach for treating neurodegenerative diseases. This review describes the role of mitochondrial abnormalities and over-activated inflammasomes in the progression of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), Multiple sclerosis (MS), Amyotrophic lateral sclerosis (ALS), and Friedrich ataxia (FRDA). We also discuss the therapeutic strategies focusing on signaling pathways associated with inflammasome activation, which potentially alleviate neurodegenerative symptoms and impede disease progression.
引用
收藏
页码:72 / 83
页数:12
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