Endoplasmic Reticulum Stress and Type 2 Diabetes
Year: 2012
Type: review
Abstract: Given the functional importance of the endoplasmic reticulum (ER), an organelle that performs folding, modification, and trafficking of secretory and membrane proteins to the Golgi compartment, the maintenance of ER homeostasis in insulin-secreting β-cells is very important. When ER homeostasis is disrupted, the ER generates adaptive signaling pathways, called the unfolded protein response (UPR), to maintain homeostasis of this organelle. However, if homeostasis fails to be restored, the ER initiates death signaling pathways. New observations suggest that both chronic hyperglycemia and hyperlipidemia, known as important causative factors of type 2 diabetes (T2D), disrupt ER homeostasis to induce unresolvable UPR activation and β-cell death. This review examines how the UPR pathways, induced by high glucose and free fatty acids (FFAs), interact to disrupt ER function and cause β-cell dysfunction and death.
Source: Annual Review of Biochemistry
Authors: Sung Hoon Back, Randal J. Kaufman
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: green
Awards: Regulation of ER stress-induced cell death, Unfolded Protein Response in Glucose Homeostasis, Alteration in protein interactions with proinsulin and insulin in type 2 diabetes, Regulation of Factor FVIII Secretion, G4107735943, TRANSLATIONAL CONTROL IN REGULATION OF APOPTOSIS, Molecular Genetics of Coagulation Disorders, Role of the Unfolded Protein Response in Beta Cell
OpenAlex ID: W2165266278