Ortiz A, Lorz C, Justo P, Catalán M P, Egido J
Unidad de Dialisis, Fundacion Jimenez Diaz, Av Reyes Catolicos 2, 28040 Madrid, Spain.
J Cell Mol Med. 2001 Jan-Mar;5(1):18-32. doi: 10.1111/j.1582-4934.2001.tb00135.x.
Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The role of apoptosis ranges from induction to repair and progression of renal injury. Death ligands and receptors, such as TNF and FasL, proapoptotic and antiapoptotic Bcl-2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal injury. These proteins represent potential therapeutic targets, which should be further explored.
细胞数量异常在肾脏疾病中很常见,范围从感染后肾小球肾炎的细胞增多到慢性肾萎缩的细胞减少。最近的研究表明,细胞凋亡及其调节机制有助于肾脏中的细胞数量调节。细胞凋亡的作用范围从肾损伤的诱导到修复和进展。死亡配体和受体,如肿瘤坏死因子(TNF)和Fas配体(FasL)、促凋亡和抗凋亡的Bcl-2家族成员以及半胱天冬酶,均已证实在肾损伤过程中参与细胞凋亡调节。这些蛋白质代表了潜在的治疗靶点,应进一步探索。