Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy
Purpose of Review. Describing the diverse molecular mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus. Recent Findings. Beta cell death is the final event in a series of mechanisms that, up to date, have not been entirely...
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Format: | Article |
Language: | English |
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Wiley
2018-01-01
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Series: | Journal of Diabetes Research |
Online Access: | http://dx.doi.org/10.1155/2018/9601801 |
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author | Joselyn Rojas Valmore Bermudez Jim Palmar María Sofía Martínez Luis Carlos Olivar Manuel Nava Daniel Tomey Milagros Rojas Juan Salazar Carlos Garicano Manuel Velasco |
author_facet | Joselyn Rojas Valmore Bermudez Jim Palmar María Sofía Martínez Luis Carlos Olivar Manuel Nava Daniel Tomey Milagros Rojas Juan Salazar Carlos Garicano Manuel Velasco |
author_sort | Joselyn Rojas |
collection | DOAJ |
description | Purpose of Review. Describing the diverse molecular mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus. Recent Findings. Beta cell death is the final event in a series of mechanisms that, up to date, have not been entirely clarified; it represents the pathophysiological mechanism in the natural history of diabetes mellitus. These mechanisms are not limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus. They also include the action of proinflammatory cytokines, the production of reactive oxygen species, DNA fragmentation (typical of necroptosis in type 1 diabetic patients), excessive production of islet amyloid polypeptide with the consequent endoplasmic reticulum stress, disruption in autophagy mechanisms, and protein complex formation, such as the inflammasome, capable of increasing oxidative stress produced by mitochondrial damage. Summary. Necroptosis, autophagy, and pyroptosis are molecular mechanisms that modulate the survival of the pancreatic beta cell, demonstrating the importance of the immune system in glucolipotoxicity processes and the potential role for immunometabolism as another component of what once known as the “ominous octet.” |
format | Article |
id | doaj-art-763210ef873a42f98b5c49b48293627e |
institution | Kabale University |
issn | 2314-6745 2314-6753 |
language | English |
publishDate | 2018-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Diabetes Research |
spelling | doaj-art-763210ef873a42f98b5c49b48293627e2025-02-03T01:22:47ZengWileyJournal of Diabetes Research2314-67452314-67532018-01-01201810.1155/2018/96018019601801Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes TherapyJoselyn Rojas0Valmore Bermudez1Jim Palmar2María Sofía Martínez3Luis Carlos Olivar4Manuel Nava5Daniel Tomey6Milagros Rojas7Juan Salazar8Carlos Garicano9Manuel Velasco10Pulmonary and Critical Care Medicine Department, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USAEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaEndocrine and Metabolic Research Center, University of Zulia, Maracaibo, VenezuelaGrupo de Investigación Altos Estudios de Frontera (ALEF), Universidad Simón Bolívar, Cúcuta, ColombiaClinical Pharmacology Unit. School of Medicine José María Vargas, Central University of Venezuela, Caracas, VenezuelaPurpose of Review. Describing the diverse molecular mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus. Recent Findings. Beta cell death is the final event in a series of mechanisms that, up to date, have not been entirely clarified; it represents the pathophysiological mechanism in the natural history of diabetes mellitus. These mechanisms are not limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus. They also include the action of proinflammatory cytokines, the production of reactive oxygen species, DNA fragmentation (typical of necroptosis in type 1 diabetic patients), excessive production of islet amyloid polypeptide with the consequent endoplasmic reticulum stress, disruption in autophagy mechanisms, and protein complex formation, such as the inflammasome, capable of increasing oxidative stress produced by mitochondrial damage. Summary. Necroptosis, autophagy, and pyroptosis are molecular mechanisms that modulate the survival of the pancreatic beta cell, demonstrating the importance of the immune system in glucolipotoxicity processes and the potential role for immunometabolism as another component of what once known as the “ominous octet.”http://dx.doi.org/10.1155/2018/9601801 |
spellingShingle | Joselyn Rojas Valmore Bermudez Jim Palmar María Sofía Martínez Luis Carlos Olivar Manuel Nava Daniel Tomey Milagros Rojas Juan Salazar Carlos Garicano Manuel Velasco Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy Journal of Diabetes Research |
title | Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy |
title_full | Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy |
title_fullStr | Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy |
title_full_unstemmed | Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy |
title_short | Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy |
title_sort | pancreatic beta cell death novel potential mechanisms in diabetes therapy |
url | http://dx.doi.org/10.1155/2018/9601801 |
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