Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus
Ferroptosis is a novel form of nonapoptotic regulated cell death (RCD). It features iron-dependent lipid peroxide accumulation accompanied by inadequate redox enzymes, especially glutathione peroxidase 4 (GPX4). RAS-selective lethal 3 (RSL3), erastin, and ferroptosis inducing 56 (FIN56) induce ferro...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2021-01-01
|
| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2021/9999612 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832561457567367168 |
|---|---|
| author | Wenxin Sha Fei Hu Yang Xi Yudong Chu Shizhong Bu |
| author_facet | Wenxin Sha Fei Hu Yang Xi Yudong Chu Shizhong Bu |
| author_sort | Wenxin Sha |
| collection | DOAJ |
| description | Ferroptosis is a novel form of nonapoptotic regulated cell death (RCD). It features iron-dependent lipid peroxide accumulation accompanied by inadequate redox enzymes, especially glutathione peroxidase 4 (GPX4). RAS-selective lethal 3 (RSL3), erastin, and ferroptosis inducing 56 (FIN56) induce ferroptosis via different manners targeting GPX4 function. Acyl-CoA synthetase long-chain family 4 (ACSL4), lysophosphatidylcholine acyltransferase 3 (LPCAT3), and lipoxygenases (LOXs) participate in the production of lipid peroxides. Heat shock protein family B member 1 (HSPB1) and nuclear receptor coactivator 4 (NCOA4) regulate iron homeostasis preventing ferroptosis caused by the high concentration of intracellular iron. Ferroptosis is ubiquitous in our body as it exists in both physiologic and pathogenic processes. It is involved in glucose-stimulated insulin secretion (GSIS) impairment and arsenic-induced pancreatic damage in the pathogenesis of diabetes. Moreover, iron and the iron-sulfur (Fe-S) cluster influence each other, causing mitochondrial iron accumulation, more reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, failure in biosynthesis of insulin, and ferroptosis in β-cells. In addition, ferroptosis also engages in the pathogenesis of diabetic complications such as myocardial ischemia and diabetic cardiomyopathy (DCM). In this review, we summarize the mechanism of ferroptosis and especially its association with type 2 diabetes mellitus (T2DM). |
| format | Article |
| id | doaj-art-c7b503ae67af4fa58833a4e8a59530a9 |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-c7b503ae67af4fa58833a4e8a59530a92025-02-03T01:25:07ZengWileyJournal of Diabetes Research2314-67452314-67532021-01-01202110.1155/2021/99996129999612Mechanism of Ferroptosis and Its Role in Type 2 Diabetes MellitusWenxin Sha0Fei Hu1Yang Xi2Yudong Chu3Shizhong Bu4Diabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, ChinaDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, ChinaDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, ChinaDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, ChinaDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, ChinaFerroptosis is a novel form of nonapoptotic regulated cell death (RCD). It features iron-dependent lipid peroxide accumulation accompanied by inadequate redox enzymes, especially glutathione peroxidase 4 (GPX4). RAS-selective lethal 3 (RSL3), erastin, and ferroptosis inducing 56 (FIN56) induce ferroptosis via different manners targeting GPX4 function. Acyl-CoA synthetase long-chain family 4 (ACSL4), lysophosphatidylcholine acyltransferase 3 (LPCAT3), and lipoxygenases (LOXs) participate in the production of lipid peroxides. Heat shock protein family B member 1 (HSPB1) and nuclear receptor coactivator 4 (NCOA4) regulate iron homeostasis preventing ferroptosis caused by the high concentration of intracellular iron. Ferroptosis is ubiquitous in our body as it exists in both physiologic and pathogenic processes. It is involved in glucose-stimulated insulin secretion (GSIS) impairment and arsenic-induced pancreatic damage in the pathogenesis of diabetes. Moreover, iron and the iron-sulfur (Fe-S) cluster influence each other, causing mitochondrial iron accumulation, more reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, failure in biosynthesis of insulin, and ferroptosis in β-cells. In addition, ferroptosis also engages in the pathogenesis of diabetic complications such as myocardial ischemia and diabetic cardiomyopathy (DCM). In this review, we summarize the mechanism of ferroptosis and especially its association with type 2 diabetes mellitus (T2DM).http://dx.doi.org/10.1155/2021/9999612 |
| spellingShingle | Wenxin Sha Fei Hu Yang Xi Yudong Chu Shizhong Bu Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus Journal of Diabetes Research |
| title | Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus |
| title_full | Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus |
| title_fullStr | Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus |
| title_full_unstemmed | Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus |
| title_short | Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus |
| title_sort | mechanism of ferroptosis and its role in type 2 diabetes mellitus |
| url | http://dx.doi.org/10.1155/2021/9999612 |
| work_keys_str_mv | AT wenxinsha mechanismofferroptosisanditsroleintype2diabetesmellitus AT feihu mechanismofferroptosisanditsroleintype2diabetesmellitus AT yangxi mechanismofferroptosisanditsroleintype2diabetesmellitus AT yudongchu mechanismofferroptosisanditsroleintype2diabetesmellitus AT shizhongbu mechanismofferroptosisanditsroleintype2diabetesmellitus |