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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation

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Author(s):
Meyerovich, Kira ; Ortis, Fernanda ; Allagnat, Florent ; Cardozo, Alessandra K.
Total Authors: 4
Document type: Review article
Source: JOURNAL OF MOLECULAR ENDOCRINOLOGY; v. 57, n. 1, p. R1-R17, JUL 2016.
Web of Science Citations: 23
Abstract

Insulin-secreting pancreatic beta-cells are extremely dependent on their endoplasmic reticulum ( ER) to cope with the oscillatory requirement of secreted insulin to maintain normoglycemia. Insulin translation and folding rely greatly on the unfolded protein response ( UPR), an array of three main signaling pathways designed to maintain ER homeostasis and limit ER stress. However, prolonged or excessive UPR activation triggers alternative molecular pathways that can lead to beta-cell dysfunction and apoptosis. An increasing number of studies suggest a role of these pro-apoptotic UPR pathways in the downfall of beta-cells observed in diabetic patients. Particularly, the past few years highlighted a cross talk between the UPR and inflammation in the context of both type 1 ( T1D) and type 2 diabetes ( T2D). In this article, we describe the recent advances in research regarding the interplay between ER stress, the UPR, and inflammation in the context of beta-cell apoptosis leading to diabetes. (AU)

FAPESP's process: 10/05587-1 - Study of the differential NF-kB activation in beta cells and the mechanisms that can be modulated for the prevention of its pro-apoptotic effect
Grantee:Fernanda Ortis
Support Opportunities: Research Grants - Young Investigators Grants