首页|Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis

Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis

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Renal fibrosis is a devastating consequence of progressive chronic kidney disease,representing a major public health challenge worldwide.The underlying mechanisms in the pathogenesis of renal fibrosis remain unclear,and effective treatments are still lacking.Renal tubular epithelial cells(RTECs)maintain kidney function,and their dysfunction has emerged as a critical contributor to renal fibrosis.Cellular quality control comprises several components,including telomere homeostasis,ubiquitin-proteasome system(UPS),autophagy,mitochondrial homeostasis(mitophagy and mitochondrial metabolism),endoplasmic reticulum(ER,unfolded protein response),and lysosomes.Failures in the cellular quality control of RTECs,including DNA,protein,and organelle damage,exert profibrotic functions by leading to senescence,defective autophagy,ER stress,mitochondrial and lysosomal dysfunction,apoptosis,fibro-blast activation,and immune cell recruitment.In this review,we summarize recent advances in un-derstanding the role of quality control components and intercellular crosstalk networks in RTECs,within the context of renal fibrosis.

Renal tubular epithelial cellsQuality controlRenal fibrosisTelomere homeostasisAutophagyMitochondria

Yini Bao、Qiyuan Shan、Keda Lu、Qiao Yang、Ying Liang、Haodan Kuang、Lu Wang、Min Hao、Mengyun Peng、Shuosheng Zhang、Gang Cao

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School of Pharmacy,Zhejiang Chinese Medical University,Hangzhou 310053,China

The Third Affiliated Hospital of Zhejiang Chinese Medical University,Hangzhou 310009,China

College of Chinese Materia Medica and Food Engineering,Shanxi University of Chinese Medicine,Jinzhong,Shanxi,030600,China

School of Pharmacy,Zhejiang Chinese Medical University,Hangzhou,310053,China

The Third Affiliated Hospital of Zhejiang Chinese Medical University,Hangzhou,310009,China

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2024

药物分析学报(英文)
西安交通大学

药物分析学报(英文)

影响因子:0.244
ISSN:2095-1779
年,卷(期):2024.14(8)