Epithelial proliferation and cell cycle dysregulation in kidney injury and disease

被引:37
|
作者
Lee, Kyung [1 ]
Gusella, G. Luca [1 ]
He, John Cijiang [1 ,2 ]
机构
[1] Icahn Sch Med Mt Sinai, Div Nephrol, Dept Med, Box 1243,One Gustave L Levy Pl, New York, NY 10029 USA
[2] James J Peters Vet Affairs Med Ctr, Renal Program, Bronx, NY USA
基金
美国国家卫生研究院;
关键词
acute kidney injury; cell cycle; HIV-associated nephropathy; polycystic kidney disease; renal tubular epithelial cells; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; HIV-ASSOCIATED NEPHROPATHY; OF-FUNCTION MODEL; PROXIMAL TUBULE; CDK INHIBITORS; CYST FORMATION; TRANSCRIPTIONAL REPRESSOR; MOLECULAR-MECHANISMS; ACCESSORY PROTEINS; VOLUME PROGRESSION;
D O I
10.1016/j.kint.2021.03.024
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Various cellular insults and injury to renal epithelial cells stimulate repair mechanisms to adapt and restore the organ homeostasis. Renal tubular epithelial cells are endowed with regenerative capacity, which allows for a restoration of nephron function after acute kidney injury. However, recent evidence indicates that the repair is often incomplete, leading to maladaptive responses that promote the progression to chronic kidney disease. The dysregulated cell cycle and proliferation is also a key feature of renal tubular epithelial cells in polycystic kidney disease and HIV-associated nephropathy. Therefore, in this review, we provide an overview of cell cycle regulation and the consequences of dysregulated cell proliferation in acute kidney injury, polycystic kidney disease, and HIV-associated nephropathy. An increased understanding of these processes may help define better targets for kidney repair and combat chronic kidney disease progression.
引用
收藏
页码:67 / 78
页数:12
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