title: Contribution of apoptotic cell death to renal injury.
abstract: 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.
authors.affiliation: Unidad de Dialisis, Fundacion Jimenez Diaz, Av Reyes Catolicos 2, 28040 Madrid, Spain. aortiz@fjd.es
authors.forename: A
authors.initials: A
authors.lastname: Ortiz
authors.forename: C
authors.initials: C
authors.lastname: Lorz
authors.forename: P
authors.initials: P
authors.lastname: Justo
authors.forename: M P
authors.initials: MP
authors.lastname: Catalán
authors.forename: J
authors.initials: J
authors.lastname: Egido
mesh_terms: D000818:Animals; D017209:Apoptosis; D020169:Caspases / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000473:pathology*; D007674:Kidney Diseases / Q000473:pathology*; D008928:Mitochondria / Q000201:enzymology; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism
chemical_list: D016207:Cytokines; D018124:Receptors, Tumor Necrosis Factor; D020169:Caspases