Apoptosis in polycystic kidney disease.
Apoptosis is the process of programmed cell death. It is a ubiquitous, controlled process consuming cellular energy and designed to avoid cytokine release despite activation of local immune cells, which clear the cell fragments. The process occurs during organ development and in maintenance of homeostasis. Abnormalities in any step of the apoptotic process are associated with autoimmune diseases and malignancies. Polycystic kidney disease (PKD) is the most common inherited kidney disease leading to end-stage renal disease (ESRD). Cyst formation requires multiple mechanisms and apoptosis is considered one of them. Abnormalities in apoptotic processes have been described in various murine and rodent models of PKD as well as in human PKD kidneys. The purpose of this review is to outline the role of apoptosis in progression of PKD as well as to describe the mechanisms involved. This article is part of a Special Issue entitled: Polycystic Kidney Disease.
Albert Einstein College of Medicine, Bronx, NY, USA. bgoilav@montefiore.org
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Goilav
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D061945:Caspase Inhibitors; D020169:Caspases / Q000502:physiology; D002453:Cell Cycle; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors; D006801:Humans; D051379:Mice; D015233:Models, Statistical; D007690:Polycystic Kidney Diseases / Q000188:drug therapy / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D011519:Proto-Oncogenes; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors; D050396:TRPP Cation Channels / Q000502:physiology
D061945:Caspase Inhibitors; D050396:TRPP Cation Channels; D058570:TOR Serine-Threonine Kinases; D018844:Cyclin-Dependent Kinases; D020169:Caspases