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Pathological β-Cell Endoplasmic Reticulum Stress in Type 2 Diabetes: Current Evidence
Neha Shrestha1, Elisa De Franco2, Peter Arvan1,3
1Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, United States.
Frontiers in Endocrinology
|May 10, 2021
Summary
Endoplasmic reticulum (ER) stress is present in diabetes, but its role in pancreatic beta-cell failure is debated. Experts review evidence suggesting a regulated unfolded protein response (UPR) is vital for beta-cell health, but prolonged stress is detrimental.
Area of Science:
- Endocrinology
- Molecular Biology
- Cellular Biology
Background:
- Pancreatic beta-cells in diabetes exhibit endoplasmic reticulum (ER) stress markers.
- The precise role of ER stress in beta-cell failure in type 2 diabetes remains controversial.
Purpose of the Study:
- To review and reconcile expert views on the role of ER stress in monogenic and type 2 diabetes.
- To evaluate whether ER stress is a cause of beta-cell failure or an adaptive response.
Main Methods:
- Expert review of existing scientific evidence.
- Analysis of data concerning ER stress and unfolded protein response (UPR) in diabetes models.
Main Results:
- A regulated UPR is essential for beta-cell development, function, and survival.
- Prolonged ER stress signaling can be detrimental to beta-cells.
Conclusions:
- The unfolded protein response (UPR) plays a critical role in maintaining beta-cell homeostasis.
- Achieving an "optimal" UPR is crucial for ER homeostasis, beta-cell function, and survival in diabetes.
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