Calcium is a highly positively charged ionic species. It regulates all cell types' functions and is an important second messenger that controls and triggers several mechanisms, including membrane stabilization, permeability, contraction, secretion, mitosis, intercellular communications, and in the activation of kinases and gene expression. Therefore, controlling calcium transport and its intracellular homeostasis in physiology leads to the healthy functioning of the biological system. However, abnormal extracellular and intracellular calcium homeostasis leads to cardiovascular, skeletal, immune, secretory diseases, and cancer. Therefore, the pharmacological control of calcium influx directly via calcium channels and exchangers and its outflow via calcium pumps and uptake by the ER/SR are crucial in treating calcium transport remodeling in pathology. Here, we mainly focused on selective calcium transporters and blockers in the cardiovascular system.
Keywords: Cav1; Cav2; Cav3; G protein; GPCR; L-type calcium channel; N-type calcium channel; P/Q-type calcium channel; R-type calcium channel; T-type calcium channel; calcium; calcium channel blockers; calcium homeostasis; calcium overload; calcium pumps; endoplasmic reticulum; hypercalcemia; mitochondria; nucleus; sodium/calcium exchanger.