Beth Israel Deaconess Medical Center and Harvard Medical School, Division of Nephrology, Boston, Massachusetts, USA.
Kidney Int. 2017 Apr;91(4):773-775. doi: 10.1016/j.kint.2016.12.033.
Fibrosis is a common response to injury but can also perpetuate tissue dysfunction. Transient receptor potential C6 (TRPC6) is implicated in cardiac and skin healing via regulation of myofibroblast differentiation. Wu et al. now demonstrate a role for TRPC6 in renal fibrosis, via a mechanism that also relies on TRPC3 and is antagonized by soluble klotho. Modulation of TRPC3/6 activity may provide a means of dampening the fibrotic response involved in chronic kidney disease progression.
纤维化是一种常见的损伤反应，但也会导致组织功能障碍。瞬时受体电位 C6（TRPC6）通过调节成肌纤维细胞分化参与心脏和皮肤愈合。Wu 等人现在证明了 TRPC6 在肾脏纤维化中的作用，其机制也依赖于 TRPC3 ，并受到可溶性 klotho 的拮抗。TRPC3/6 活性的调节可能为抑制慢性肾脏病进展中涉及的纤维化反应提供一种手段。
