期刊
FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.1028130
关键词
type 1 diabetes; glucose metabolism; posttranslational modifications; biomarkers; neoepitopes
类别
资金
- JDRF [3-SRA-2017-345-S-B, 1-SRA-2020-977-S-B, 1-INO-2022-1116-A-N]
- NIH
This article summarizes the potential pathological consequences of posttranslational protein modifications (PTMs) and their associated biomarkers in the autoimmune disease type 1 diabetes (T1D), as well as the preventive and therapeutic approaches targeting PTMs to restore normal metabolic pathways in pancreatic islets.
Posttranslational protein modifications (PTMs) are an inherent response to physiological changes causing altered protein structure and potentially modulating important biological functions of the modified protein. Besides cellular metabolic pathways that may be dictated by PTMs, the subtle change of proteins also may provoke immune attack in numerous autoimmune diseases. Type 1 diabetes (T1D) is a chronic autoimmune disease destroying insulin-producing beta cells within the pancreatic islets, a result of tissue inflammation to specific autoantigens. This review summarizes how PTMs arise and the potential pathological consequence of PTMs, with particular focus on specific autoimmunity to pancreatic beta cells and cellular metabolic dysfunction in T1D. Moreover, we review PTM-associated biomarkers in the prediction, diagnosis and in monitoring disease activity in T1D. Finally, we will discuss potential preventive and therapeutic approaches of targeting PTMs in repairing or restoring normal metabolic pathways in pancreatic islets.
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