A choice of death – the signal-transduction of immune-mediated beta-cell apoptosis

By Decio L. Eizirik, T. Mandrup-Poulsen. Diabetologia, 2001

929 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Surgery

View Paper: https://www.semanticscholar.org/paper/db67fce7b96768661450e12174a77aaf1a8da100

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Citations in the corpus

The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “Cytokine-induced death in human, rat, and mouse -cells, and in insulin-producing cell lines, occurs mostly by apoptosis (2, 25, 226), but there is also a minor NO-dependent necrotic component in rodent -cells (227).”
Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “It does so through activation of the transcription factor NF-κB which is responsible for the induction of iNOS and subsequent production of NO• [155, 221].”
The role of inflammation in insulitis and β-cell loss in type 1 diabetes (2009, background): “In T1DM, local, pancreatic-islet inflammation (insulitis) contributes to the progressive loss of insulin-producing β cells, which eventually renders the patients—many of them children or adolescents—insulin-dependent for life”
Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, neutral): “N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript RRP Readily releasable pool SERCA-2b Sarcoendoplasmic reticulum Ca2+ ATPase type 2b SHP Small heterodimer partner SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptor SOD Superoxide dismutase S”
Chronic palmitate but not oleate exposure induces endoplasmic reticulum stress, which may contribute to INS-1 pancreatic beta-cell apoptosis. (2006, background): “Inflammatory cytokines such as TNF , IL-1 , and interferon- have been shown to be cytotoxic to -cells (3) and may contribute to -cell death in obesity, which has been described as a state of low-level chronic inflammation (4).”
Roles of CHOP/GADD153 in endoplasmic reticulum stress (2004, background): “Studies on islet cells lacking PARP and p53-negative cells suggested an apoptosis pathway distinct from the DNA damage pathway.(80,81) We found that NO causes ER stress by depleting ER Ca2þ stores and leads to apoptosis in b-cells via CHOP induction (Figure 4a).”