Bhardwaj Rajesh, Parekh Anant B
Molecular & Cellular Biology Laboratory, National Institute of Environmental Health Sciences, National Institute of Health, Durham, USA.
Biochem Soc Trans. 2025 Jun 30;53(3):627-642. doi: 10.1042/BST20253062.
A rise in cytosolic Ca2+ is used as a key signalling messenger in eukaryotic cells. The Ca2+ signal drives life and death and controls myriad responses in between. Inherent in the use of such a multifarious signal is the danger of disease, arising from dysregulated Ca2+ signalling. One ancient, highly conserved and widespread Ca2+ entry pathway is the store-operated Ca2+ release-activated Ca2+ (CRAC) channel. Mutations in STIM1 and ORAI1, the genes that encode the functional channel, are tightly linked to a CRAC channelopathy in humans, which encompasses severe combined immune deficiency, myopathy and anhidrotic ectodermal dysplasia. Moreover, sustained Ca2+ entry through the channels leads to a range of systemic disorders, including acute pancreatitis, asthma and inflammatory bowel disease. In this review, we describe how aberrant CRAC channel activity causes a range of diseases, highlighting commonalities between these diverse pathologies.
胞质Ca2+浓度升高是真核细胞中关键的信号信使。Ca2+信号决定细胞生死,并控制其间的无数反应。使用如此多样的信号所固有的风险是,Ca2+信号失调会引发疾病。一种古老、高度保守且广泛存在的Ca2+内流途径是储存-操纵性Ca2+释放激活Ca2+(CRAC)通道。编码功能性通道的基因STIM1和ORAI1发生突变,与人类CRAC通道病紧密相关,该病包括严重联合免疫缺陷、肌病和无汗性外胚层发育不良。此外,通过这些通道持续的Ca2+内流会导致一系列全身性疾病,包括急性胰腺炎、哮喘和炎症性肠病。在本综述中,我们描述了异常的CRAC通道活性如何导致一系列疾病,强调了这些不同病理之间的共性。