Advances in Islet Biology: A Themed Issue in Honor of Prof. Claes B. Wollheim
A Special Issue of Biomolecules (ISSN 2218-273X) belonging to the section "Molecular Biology".
Deadline for manuscript submissions: 30 June 2027 | Viewed by 88
Editor
Interests: β-cell dysfunction; noncoding RNAs; islet
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Dysfunction of the insulin-secreting pancreatic islet beta cells is the central mechanism in the development of both autoimmune type 1 and life-style-related type 2 diabetes. Professor Claes Wollheim has devoted more than five decades of research to elucidating beta-cell function in health and disease. This Special Issue of Biomolecules will address the multitude of physiological and pathophysiological findings that have led to remarkable advances in our understanding of signal transduction underlying nutrient-stimulated insulin secretion and its regulation by the neighboring glucagon-secreting alpha cell. Insulin secretion derangements in both polygenic type 2 and monogenic forms of diabetes, as well as beta-cell demise in type 1 diabetes, will be highlighted. The high energy demands of the beta cell require efficient ATP production by mitochondria, whose oxidative phosphorylation is enhanced by calcium, a crucial intracellular messenger in the metabolism–secretion coupling of insulin release. Normal mitochondrial function depends on a dynamic balance between biogenesis and degradation through autophagy and mitophagy. The sensitivity of beta-cell mitochondria to oxidative stress and calcium overload makes them particularly susceptible to cellular stress, in turn disrupting bioenergetics and blunting glucose-stimulated insulin secretion, eventually leading to various forms of cell death. Elucidating the mechanisms underlying beta-cell pathophysiology should facilitate the development of novel therapeutic approaches for all forms of diabetes.
Prof. Dr. Romano Regazzi
Guest Editor
Manuscript Submission Information
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Keywords
- diabetes
- beta cell
- insulin secretion
- mitochondria
- calcium signaling
- cell death
- circadian rhythms
- metabolism–secretion coupling
- proinsulin biosynthesis
- inflammation
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