Research conducted over the last two decades has dramatically advanced the understanding of store-operated calcium channels (SOCC) and their impact on renal function. Kidneys contain many types of cells, including those specialized for glomerular filtration (fenestrated capillary endothelium, podocytes), water and solute transport (tubular epithelium), and regulation of glomerular filtration and renal blood flow (vascular smooth muscle cells, mesangial cells). The highly integrated function of these myriad cells effects renal control of blood pressure, extracellular fluid volume and osmolality, electrolyte balance, and acid–base homeostasis. Many of these cells are regulated by Ca²⁺ signaling. Recent evidence demonstrates that SOCCs are major Ca²⁺ entry portals in several renal cell types. SOCC is activated by depletion of Ca²⁺ stores in the sarco/endoplasmic reticulum, which communicates with plasma membrane SOCC via the Ca²⁺ sensor Stromal Interaction Molecule 1 (STIM1). Orai1 is recognized as the main pore-forming subunit of SOCC in the plasma membrane. Orai proteins alone can form highly Ca²⁺ selective SOCC channels. Also, members of the Transient Receptor Potential Canonical (TRPC) channel family are proposed to form heteromeric complexes with Orai1 subunits, forming SOCC with low Ca²⁺ selectivity. Recently, Ca²⁺ entry through SOCC, known as store-operated Ca²⁺ entry (SOCE), was identified in glomerular mesangial cells, tubular epithelium, and renovascular smooth muscle cells. The physiological and pathological relevance and the characterization of SOCC complexes in those cells are still unclear. In this review, we summarize the current knowledge of SOCC and their roles in renal glomerular, tubular and vascular cells, including studies from our laboratory, emphasizing SOCE regulation of fibrotic protein deposition. Understanding the diverse roles of SOCE in different renal cell types is essential, as SOCC and its signaling pathways are emerging targets for treatment of SOCE-related diseases.

在过去的二十年中进行的研究极大地促进了对储存操作的钙通道 (SOCC) 及其对肾功能的影响的理解。肾脏包含许多类型的细胞，包括专门用于肾小球滤过（有孔的毛细血管内皮、足细胞）、水和溶质转运（肾小管上皮）以及调节肾小球滤过和肾血流（血管平滑肌细胞、系膜细胞）的细胞。这些无数细胞的高度整合功能影响肾脏对血压、细胞外液体积和渗透压、电解质平衡和酸碱平衡的控制。许多这些细胞受Ca ²⁺信号传导的调节。最近的证据表明 SOCC 是主要的 Ca ²⁺几种肾细胞类型的入口。SOCC 被肌组织/内质网中 Ca ^{2+储存的消耗激活，该内质网通过 Ca 2+}传感器基质相互作用分子 1 (STIM1)与质膜 SOCC 通信。Orai1 被认为是质膜中 SOCC 的主要成孔亚基。Orai 蛋白单独可以形成高度 Ca ²⁺选择性 SOCC 通道。此外，瞬时受体电位规范 (TRPC) 通道家族的成员被提议与 Orai1 亚基形成异聚复合物，形成具有低 Ca ²⁺选择性的 SOCC。最近，Ca ²⁺通过 SOCC 进入，称为存储操作的 Ca ²⁺进入（SOCE），在肾小球系膜细胞、肾小管上皮和肾血管平滑肌细胞中发现。这些细胞中 SOCC 复合物的生理和病理相关性以及表征仍不清楚。在这篇综述中，我们总结了 SOCC 的当前知识及其在肾小球、肾小管和血管细胞中的作用，包括我们实验室的研究，强调 SOCC 对纤维化蛋白沉积的调节。了解 SOCE 在不同肾细胞类型中的不同作用至关重要，因为 SOCC 及其信号通路是治疗 SOCE 相关疾病的新兴靶点。