Edelstein Charles L
Division of Renal Diseases and Hypertension, University of Colorado School of Medicine, Denver, Colorado 80262, USA.
Cell Cycle. 2005 Nov;4(11):1550-4. doi: 10.4161/cc.4.11.2185. Epub 2005 Nov 17.
Tubular epithelial cell apoptosis occurs in most animal models of polycystic kidney disease (PKD) and in kidneys from humans with autosomal dominant polycystic kidney disease (ADPKD). Induction of apoptosis in cultured tubular epithelial cells results in cyst formation. Induction of apoptosis in the kidney in Bcl-2 deficient mice results in increased proliferation of tubular epithelium and cyst formation. Caspase inhibition reduces tubular apoptosis and proliferation and slows disease progression in the Han:SPRD rat model of PKD. Thus, there is evidence that both epithelial cell apoptosis and proliferation are dysregulated in ADPKD and may represent a general mechanism for cyst growth.
在大多数多囊肾病（PKD）动物模型以及患有常染色体显性多囊肾病（ADPKD）的人类肾脏中，都会发生肾小管上皮细胞凋亡。在培养的肾小管上皮细胞中诱导凋亡会导致囊肿形成。在Bcl-2基因缺陷小鼠的肾脏中诱导凋亡会导致肾小管上皮细胞增殖增加以及囊肿形成。在PKD的Han:SPRD大鼠模型中，半胱天冬酶抑制可减少肾小管凋亡和增殖，并减缓疾病进展。因此，有证据表明ADPKD中上皮细胞凋亡和增殖均失调，这可能是囊肿生长的普遍机制。
