期刊
ARQUIVOS BRASILEIROS DE ENDOCRINOLOGIA E METABOLOGIA
卷 52, 期 2, 页码 156-165出版社
SBEM-SOC BRASIL ENDOCRINOLOGIA & METABOLOGIA
DOI: 10.1590/S0004-27302008000200003
关键词
pancreatic beta-cell; diabetes mellitus; apoptosis; cytokines; endoplasmic reticulum; ER stress
Type 1 diabetes mellitus (T1D) is characterized by severe insulin deficiency resulting from chronic and progressive destruction of pancreatic beta-cells by the immune system. The triggering of autoimmunity against the beta-cells is probably caused by environmental agent(s) acting in the context of a predisposing genetic background. Once activated, the immune cells invade the islets and mediate their deleterious effects on beta-cells via mechanisms such as Fas/FasL, perform/granzyme, reactive oxygen and nitrogen species and pro-inflammatory cytokines. Binding of cytokines to their receptors on the beta-cells activates MAP-kinases and the transcription factors STAT-1 and NF kappa-B, provoking functional impairment, endoplasmic reticulum stress and ultimately apoptosis. This review discusses the potential mediators and mechanisms leading to beta-cell destruction in T1D.
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