Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities.

By M. Cnop, N. Welsh, J. Jonas, A. Jörns, S. Lenzen, Decio L. Eizirik. Diabetes, 2005

1,539 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Surgery

View Paper: https://www.semanticscholar.org/paper/bc0cd007436d5930044b316a78354347427bf5a7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. M. Cerf
2. A. Gorman
3. A. K. Cardozo
4. M. Cnop
5. Afshin Samali
6. Decio L. Eizirik

In Genetics

1. M. Cnop
2. F. Ortis
3. M. Cerf
4. Decio L. Eizirik

In Surgery

1. M. Cnop
2. F. Ortis
3. M. Cerf
4. Afshin Samali
5. Decio L. Eizirik

Citations in the corpus

• Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, neutral): “Although β-cell loss is caused by excessive nutrients in T2D and an autoimmune reaction in T1D, there is a convergence in cellular signaling pathways between the two types of diabetes [268], which is schematically illustrated in Fig (2).”
• Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “In Type 2 diabetes, glucolipotoxicity, rather than proinflammatory cytokines, is considered to be an important contributing factor to β-cell dysfunction [230–234].”
• Beta Cell Dysfunction and Insulin Resistance (2013, background): “Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are formed during both cytokine-mediated proinflammatory beta cell aggression in type 1 diabetes and glucolipotoxicitymediated beta cell dysfunction in type 2 diabetes (Evans et al., 2003; Cnop et al., 2005; Robertson et al., 2007; Le”
• Initiation and execution of lipotoxic ER stress in pancreatic β-cells (2008, methodology): “At the end of all experiments, cells were lysed in a hypotonic Ca2+-rich solution (100 μM digitonin and 10 mM Ca2+ in H2O) to discharge the remaining aequorin pool for calibration of the aequorin signal (Mitchell et al., 2001).”
• Flavonoids and Their Anti-Diabetic Effects: Cellular Mechanisms and Effects to Improve Blood Sugar Levels (2019, background): “A high level of FFAs could also stimulate pro-apoptotic effects on β-cells that diminish their functions [28].”