期刊
CURRENT PROTEIN & PEPTIDE SCIENCE
卷 18, 期 12, 页码 1224-1231出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389203717666160915162238
关键词
Acute kidney injury; cell cycle arrest; insulin-like growth factor-binding protein 7; tissue inhibitor of metalloproteinase-2; pathogenesis; diagnosis
资金
- National Natural Science Foundation of China [81470975, 81400725]
- Scientific Research Program by the Science and Technology Department of Jilin Province, China [20130413029GH]
- Scientific Research Program by the Health and Family Planning Commission of Jilin Province, China [2014Z042]
The current lack of complete understanding of the pathogenesis of acute kidney injury (AKI) is a significant barrier to its early diagnosis and treatment. Cell cycle arrest plays an important role in the protection of renal tubular epithelial cells and maladaptive repair following AKI. G1 phase cell arrest serves as a protective mechanism following AKI, avoiding replication of damaged DNA. Insulinlike growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinase-2 (TIMP-2) are closely associated with G1 cell cycle arrest during the very early phase of cellular damage and can serve as an ideal biomarker to predict AKI. However, sustained cell cycle arrest after severe AKI may result in cell senescence and maladaptive repair, with typical characteristics of the development of cell cycle arrest in the gap 2 (G2) or mitotic (M) phase. Markers of cell cycle arrest signal and spread the alarm from the site of injury to adjacent cells in an autocrine or paracrine manner, giving rise to abnormal amplification and release of profibrogenic factors, activation of pericytes/perivascular fibroblasts, and eventually fibrosis. Therefore, cell cycle regulation has become a potentially new target for the prevention and treatment of AKI. In this review, we summarize the characteristics of the cell cycle following AKI and the markers of cell cycle arrest that enable the early detection of AKI. We also discuss how to prevent the progression of chronic kidney disease (CKD) by regulating cell cycle arrest.
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