Chaudhari Sarika, Ma Rong
Department of Integrative Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth 76107, TX, USA.
Department of Integrative Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth 76107, TX, USA
Exp Biol Med (Maywood). 2016 Feb;241(4):343-52. doi: 10.1177/1535370215609693. Epub 2015 Oct 14.
Store-operated Ca(2+) entry (SOCE) is mediated by the store-operated Ca(2+) channel (SOC) that opens upon depletion of internal Ca(2+) stores following activation of G protein-coupled receptors or receptor tyrosine kinases. Over the past two decades, the physiological and pathological relevance of SOCE has been extensively studied. Recently, accumulating evidence suggests associations of altered SOCE with diabetic complications. This review focuses on the implication of SOCE as it pertains to various complications resulting from diabetes. We summarize recent findings by us and others on the involvement of abnormal SOCE in the development of diabetic complications, such as diabetic nephropathy and diabetic vasculopathy. The underlying mechanisms that mediate the diabetes-associated alterations of SOCE are also discussed. The SOCE pathway may be considered as a potential therapeutic target for diabetes-associated diseases.
钙库操纵性钙内流（SOCE）由钙库操纵性钙通道（SOC）介导，该通道在G蛋白偶联受体或受体酪氨酸激酶激活后，细胞内钙库耗竭时开放。在过去二十年中，SOCE的生理和病理相关性得到了广泛研究。最近，越来越多的证据表明SOCE改变与糖尿病并发症有关。本综述重点关注SOCE与糖尿病所致各种并发症的关系。我们总结了我们自己和其他人最近关于异常SOCE参与糖尿病并发症（如糖尿病肾病和糖尿病血管病变）发生发展的研究结果。还讨论了介导与糖尿病相关的SOCE改变的潜在机制。SOCE通路可能被视为糖尿病相关疾病的潜在治疗靶点。
