粒体自噬
肾脏疾病
疾病
医学
肾
病理
生物信息学
内科学
自噬
生物
遗传学
细胞凋亡
作者
Michael Frill,Claire Thornton,Jonathan Elliott,Elisavet Vasilopoulou,Rosanne E. Jepson
标识
DOI:10.1016/j.tvjl.2025.106398
摘要
Feline chronic kidney disease (CKD) is a leading cause of mortality in older cats and though understanding of the underlying pathophysiology of this heterogenous disease is improving, many details remain elusive. Dysregulation of mitophagy, a normal cellular process whereby dysfunctional mitochondria are cleared from the cell, may contribute to ongoing inflammation, fibrosis, and ultimately worsening kidney function. Whilst advancement in the study of model species and humans have revealed differential patterns of mitophagy in the kidney in different disease states, knowledge about mitophagy in feline CKD remains unexplored. This review summarises the current knowledge based around the contribution that dysregulated mitochondrial function and mitophagy make to oxidative stress, inflammation and fibrosis in CKD, considers their potential involvement in feline CKD and how this knowledge could be used to identify potential therapeutic targets for the future.
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