坏死性下垂
裂谷1
促炎细胞因子
激酶
生物
炎症
细胞生物学
免疫学
细胞凋亡
程序性细胞死亡
遗传学
作者
Yuanxin Yang,Xingyan Li,Tao Zhang,Daichao Xu
标识
DOI:10.1093/lifemedi/lnac003
摘要
Abstract Aging is a natural process that is characterized by chronic, low-grade inflammation, which represents the primary risk factor in the pathogenesis of a variety of diseases, i.e. aging-related diseases. RIP kinases, in particular RIPK1 and RIPK3, have emerged as master regulators of proinflammatory responses that act either by causing apoptosis and necroptosis or by directly regulating intracellular inflammatory signaling. While, RIPK1/3 and necroptosis are intimately linked to multiple human diseases, the relationship among RIPK1/3, necroptosis, and aging remains unclear. In this review, we discuss current evidence arguing for the involvement of RIPK1/3 and necroptosis in the progression of aging. In addition, we provide updated information and knowledge on the role of RIPK1/3 and necroptosis in aging-related diseases. Leveraging these new mechanistic insights in aging, we postulate how our improved understanding of RIPK1/3 and necroptosis in aging may support the development of therapeutics targeting RIPK1/3 and necroptosis for the modulation of aging and treatment of aging-related diseases.
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