Li Li, Liu Youhua
State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Institute of Nephrology, Guangzhou, China.
State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Institute of Nephrology, Guangzhou, China.
Kidney Int. 2025 Apr;107(4):596-598. doi: 10.1016/j.kint.2025.01.011.
Podocyte injury causes a series of cellular changes, including hypertrophy, dedifferentiation, senescence, apoptosis, and detachment. Although evidence suggests a pivotal role of podocyte senescence in diabetic kidney disease, the exact triggers and underlying mechanism remain elusive. In this study, Li et al. uncover that GPR124, a G-protein-coupled receptor, protects against podocyte senescence by inhibiting focal adhesion kinase. These findings underscore that the GPR124/focal adhesion kinase axis could be a novel target for diabetic kidney disease therapy.
足细胞损伤会引发一系列细胞变化,包括肥大、去分化、衰老、凋亡和脱离。尽管有证据表明足细胞衰老在糖尿病肾病中起关键作用,但其确切触发因素和潜在机制仍然不明。在这项研究中,李等人发现,G蛋白偶联受体GPR124通过抑制粘着斑激酶来保护足细胞免于衰老。这些发现强调,GPR124/粘着斑激酶轴可能是糖尿病肾病治疗的一个新靶点。