1. Tubular Cell Cycle Response upon AKI: Revising Old and New Paradigms to Identify Novel Targets for CKD Prevention
- Author
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Letizia De Chiara, Carolina Conte, Elena Lazzeri, and Giulia Antonelli
- Subjects
senescence ,030232 urology & nephrology ,Review ,urologic and male genital diseases ,0302 clinical medicine ,Mitotic cell cycle ,Fibrosis ,Molecular Targeted Therapy ,Biology (General) ,Spectroscopy ,polyploidy ,0303 health sciences ,Kidney ,Cell Cycle ,Acute kidney injury ,General Medicine ,Acute Kidney Injury ,female genital diseases and pregnancy complications ,3. Good health ,Computer Science Applications ,Chemistry ,medicine.anatomical_structure ,Kidney Tubules ,cell cycle arrest ,Senescence ,medicine.medical_specialty ,QH301-705.5 ,Renal function ,Mitosis ,mitotic cell cycle ,Catalysis ,Inorganic Chemistry ,03 medical and health sciences ,alternative cell cycle ,medicine ,Animals ,Humans ,Cell Lineage ,Physical and Theoretical Chemistry ,Renal Insufficiency, Chronic ,Intensive care medicine ,Molecular Biology ,QD1-999 ,Disease burden ,030304 developmental biology ,business.industry ,urogenital system ,Organic Chemistry ,fibrosis ,Cell Cycle Checkpoints ,medicine.disease ,Histone Deacetylase Inhibitors ,acute kidney injury ,chronic kidney disease ,business ,Kidney disease - Abstract
Acute kidney injury (AKI) is characterized by a rapid deterioration of kidney function, representing a global healthcare concern. In addition, AKI survivors frequently develop chronic kidney disease (CKD), contributing to a substantial proportion of disease burden globally. Yet, over the past 30 years, the burden of CKD has not declined to the same extent as many other important non-communicable diseases, implying a substantial deficit in the understanding of the disease progression. The assumption that the kidney response to AKI is based on a high proliferative potential of proximal tubular cells (PTC) caused a critical confounding factor, which has led to a limited development of strategies to prevent AKI and halt progression toward CKD. In this review, we discuss the latest findings on multiple mechanisms of response related to cell cycle behavior of PTC upon AKI, with a specific focus on their biological relevance. Collectively, we aim to (1) provide a new perspective on interpreting cell cycle progression of PTC in response to damage and (2) discuss how this knowledge can be used to choose the right therapeutic window of treatment for preserving kidney function while avoiding CKD progression.
- Published
- 2021