Affiliation:
1. Chemical Biology Program, Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, MA 02142, USA
Abstract
Pancreatic beta-cell regeneration, for example, by inducing proliferation, remains an important goal in developing effective treatments for diabetes. However, beta cells have mainly been considered quiescent. This “static” view has recently been challenged by observations of relevant physiological conditions in which metabolic stress is compensated by an increase in beta-cell mass. Understanding the molecular mechanisms underlining these process could open the possibility of developing novel small molecules to increase beta-cell mass. Several cellular cell-cycle and signaling proteins provide attractive targets for high throughput screening, and recent advances in cell culture have enabled phenotypic screening for small molecule-induced beta-cell proliferation. We present here an overview of the current trends involving small-molecule approaches to induce beta-cell regeneration by proliferation.
Subject
Endocrine and Autonomic Systems,Endocrinology,Endocrinology, Diabetes and Metabolism
Cited by
20 articles.
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