Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Division of Nephrology, University of Washington, Seattle, Washington, USA; Institute for Stem Cell & Regenerative Medicine, University of Washington, Seattle, Washington, USA.
Kidney Int. 2022 Jul;102(1):12-13. doi: 10.1016/j.kint.2022.04.016.
Regenerative repair following injury to proximal tubular epithelial cells (PTECs) is essential to restore the kidney to normal function in acute kidney injury. Failure to accomplish this leads to chronic kidney disease. Expression of the paired-box transcription factor Pax2 in PTECs is required for their regenerative proliferation and repair. However, a loss-of-function study now shows that the absence of Pax2 not only impacts PTEC proliferation but also causes myofibroblast recruitment leading to excessive tubulointerstitial fibrosis.
损伤近端肾小管上皮细胞 (PTEC) 后的再生修复对于急性肾损伤中恢复肾脏正常功能至关重要。如果不能完成这一点,就会导致慢性肾脏病。PTEC 中配对盒转录因子 Pax2 的表达对于其再生增殖和修复是必需的。然而,一项功能丧失研究表明,Pax2 的缺失不仅会影响 PTEC 的增殖,还会导致肌成纤维细胞募集,导致过度的肾小管间质纤维化。