Endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation
| Autor: | Fernanda Ortis, Alessandra K Cardozo, Florent Allagnat, Kira Meyerovich |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
endocrine system medicine.medical_specialty Inflammasomes medicine.medical_treatment Context (language use) Inflammation Biology 03 medical and health sciences Islets of Langerhans Endocrinology Internal medicine Insulin-Secreting Cells medicine Diabetes Mellitus Animals Humans Molecular Targeted Therapy Molecular Biology Insulin Endoplasmic reticulum JNK Mitogen-Activated Protein Kinases NF-kappa B Translation (biology) Endoplasmic Reticulum Stress HISTOLOGIA Cell biology 030104 developmental biology Unfolded protein response Unfolded Protein Response Cytokines Disease Susceptibility Signal transduction medicine.symptom Inflammation Mediators Homeostasis Molecular Chaperones Signal Transduction |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| Popis: | Insulin-secreting pancreatic β-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 β-cell dysfunction and apoptosis. An increasing number of studies suggest a role of these pro-apoptotic UPR pathways in the downfall of β-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 β-cell apoptosis leading to diabetes. |
| Databáze: | OpenAIRE |
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