摘要
The nature of renal tubular cell injury in ischemic acute renal failure includes not only cell death (necrosis or apoptosis) but also sublethal injury causing cell dysfunction. The role of intracellu- lar calcium, calcium - dependent enzymes calpain, nitric oxide, phospholipase A2, loss of tubule cell polarity and tubular obstruction in the pathophysiology of the renal tubular cell injury during hypoxia/ischemia is described. The effects of vascular factors, infiltrating activited leukocytes, apoptosis and growth factors on renal tubular cell injury are discussed. Potential mechanisms that tubular injury leads to a profound fall in glomerular filtration rate are proposed.
The nature of renal tubular cell injury in ischemic acute renal failure includes not only cell death (necrosis or apoptosis) but also sublethal injury causing cell dysfunction. The role of intracellu- lar calcium, calcium - dependent enzymes calpain, nitric oxide, phospholipase A2, loss of tubule cell polarity and tubular obstruction in the pathophysiology of the renal tubular cell injury during hypoxia/ischemia is described. The effects of vascular factors, infiltrating activited leukocytes, apoptosis and growth factors on renal tubular cell injury are discussed. Potential mechanisms that tubular injury leads to a profound fall in glomerular filtration rate are proposed.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第4期377-380,共4页
Chinese Journal of Pathophysiology
