期刊
JOURNAL OF MOLECULAR BIOLOGY
卷 432, 期 5, 页码 1326-1346出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2019.08.014
关键词
-
资金
- National Institute of Health [DK097392, DK115620, DK057699, DK066485]
Ca2+ is an essential signal for pancreatic beta-cell function. Ca2+ plays critical roles in numerous beta-cell pathways such as insulin secretion, transcription, metabolism, endoplasmic reticulum function, and the stress response. Therefore, beta-cell Ca2+ handling is tightly controlled. At the plasma membrane, Ca2+ entry primarily occurs through voltage-dependent Ca2+ channels. Voltage-dependent Ca2+ channel activity is dependent on orchestrated fluctuations in the plasma membrane potential or voltage, which are mediated via the activity of many ion channels. During the pathogenesis of type 2 diabetes the beta-cell is exposed to stressful conditions, which result in alterations of Ca2+ handling. Some of the changes in beta-cell Ca2+ handling that occur under stress result from perturbations in ion channel activity, expression or localization. Defective Ca2+ signaling in the diabetic beta-cell alters function, limits insulin secretion and exacerbates hyperglycemia. In this review, we focus on the beta-cell ion channels that control Ca2+ handling and how they impact beta-cell dysfunction in type 2 diabetes. (C) 2019 Elsevier Ltd. All rights reserved.
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