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. 2022 Mar 16;9:844671. doi: 10.3389/fcvm.2022.844671

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Copyright © 2022 Wang, Xu, Wu, Shen, Lin, Fang, Zhang, Shen, Liu and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram of Orai1-mediated store-operated Ca²⁺ entry (SOCE) signal transduction pathway in human umbilical vein endothelial cells (HUVECs) after parathyroid hormone (PTH) stimulation. In this proposed mechanism, PTH acts on its receptor PTHR1, a G-protein coupled receptor, to produce phospholipase C (PLC) and then inositol triphosphate (IP₃), which stimulates its receptor to deplete Ca²⁺ stores in the endoplasmic reticulum (ER), leading to the opening of the Orai1 channel in HUVECs to induce extracellular Ca²⁺ influx via SOCE. The subsequent increase in intracellular Ca²⁺ ([Ca²⁺]_i) causes the nuclear translocation of NFATC1 through the Ca²⁺/calmodulin-dependent kinase 2 (CaMK-II)/calcineurin signaling pathway, and eventually induces COL1A1 overexpression and HUVEC migration and proliferation.