Ortiz A, Justo P, Catalán M P, Sanz A B, Lorz C, Egido J
Division of Nephrology, Fundacion Jimenez Diaz, Universidad Autonoma de Madrid, Fundacion Renal Iñigo Alvarez de Todelo, Madrid, Spain.
Curr Drug Targets Immune Endocr Metabol Disord. 2002 Jul;2(2):181-92.
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 potential role of apoptosis ranges from induction and progression to repair of renal injury. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. However, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis on the acute tubular necrosis.
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。细胞凋亡的潜在作用范围从肾损伤的诱导、进展到修复。死亡配体和受体，如肿瘤坏死因子和Fas配体、促凋亡和抗凋亡的Bcl2家族成员以及半胱天冬酶，均已被证明参与肾细胞损伤过程中的细胞凋亡调节。然而，这些蛋白质的确切作用尚不清楚，并且大多数已知的细胞凋亡调节蛋白的参与情况尚未得到研究。我们现在综述细胞凋亡在肾损伤中的作用、治疗干预的潜在分子靶点、调节这些靶点活性的治疗手段以及对细胞凋亡进行治疗干预的少数实例，重点是急性肾小管坏死。
