General calcium entry (N/A)

General calcium entry refers to the collective physiological processes by which calcium ions (Ca²⁺) move from the extracellular environment into the cytoplasm, a movement essential for cellular signaling (Berridge et al., 2003, Nature Reviews Molecular Cell Biology). This influx is mediated by several distinct classes of transmembrane proteins, including voltage-gated calcium channels (VGCCs), store-operated calcium channels (SOCE) such as Orai1, and various ligand-gated or transient receptor potential (TRP) channels (Catterall, 2011, Cold Spring Harbor Perspectives in Biology; Prakriya & Lewis, 2015, Physiological Reviews). As a ubiquitous second messenger, intracellular Ca²⁺ regulates critical functions such as muscle contraction, neurotransmitter release, and gene expression. Dysregulation of these entry pathways is a hallmark of numerous conditions, including hypertension, cardiac arrhythmias, chronic pain, and inflammatory diseases. Pharmacological targeting of general calcium entry is a well-established therapeutic strategy, most notably through the use of calcium channel blockers (CCBs) like amlodipine and verapamil for cardiovascular disorders, and newer agents targeting SOCE for conditions like acute pancreatitis (PubChem, 2024).

Other names

Calcium influxCalcium entryTransmembrane calcium transportCa2+ entryCalcium uptake

Inhibition of transmembrane calcium influx through the blockade of voltage-gated calcium channels (VGCCs), store-operated calcium channels (SOCE), or other calcium-permeable ion channels.