急性肾损伤向慢性肾脏病转化中肾小管上皮细胞损伤修复机制的研究进展

急性肾损伤(acute kidney injury, AKI)是由各种因素引起的以肾功能短期内急剧下降为主要表现的临床综合征,是慢性肾脏病(chronic kidney disease, CKD)和终末期肾脏病(end-stage renal disease, ESRD)的独立危险因素。目前对于AKI及预防AKI发展为CKD的治疗手段非常有限,发病率和病死率居高不下。因此进一步探讨AKI向CKD进展的机制,从而发现早期干预靶点变得尤为重要。在面临各种生物压力时,例如缺血、缺氧或药物毒性等,肾小管上皮细胞(renal tubular epithelial cells, RTECs)是最容易受到损伤的细胞,同时,RTECs也是驱动急性到慢性肾脏疾病进展的关键细胞。本文概述在AKI及AKI向CKD转化的过程中RTECs损伤修复的作用及机制的最新进展。

Progress on the injury and repair mechanism of renal tubular epithelial cells in the transition of acute kidney injury to chronic kidney disease

Acute kidney injury (AKI) is a clinical syndrome caused by various factors and characterized by renal function declines sharply in a short period of time. AKI, an independent risk factor of chronic kidney disease (CKD) and end-stage renal disease, is associated with high levels of morbidity and mortality. Currently, the treatments for AKI and the prevention of the transition of AKI to CKD are very limited. Therefore, it is essential to explore the mechanism of AKI to CKD. Renal tubular epithelial cells (RTECs) are the major cells of the kidney and are vulnerable to various biological stresses, such as ischemia, hypoxia and toxins.RTECs are also key inflammatory and fibrogenic cells that drive the progression from acute to chronic kidney disease. In view of the central role of RTECs, this review will focus on the maladaptive repair mechanisms of RTECs in the transition of AKI to CKD, providing novel targets and new strategies for effective treatment.