Calcium absorption in the small intestine

Calcium absorption in the small intestine is a vital process for calcium homeostasis, occurring via two primary routes: a transcellular (active, saturable, mainly in the duodenum and under hormonal regulation by vitamin D/vitamin D receptor) and a paracellular (passive, non-saturable, throughout the small intestine) pathway[1][3][4]. Key molecular players include the epithelial calcium channels TRPV6 (formerly ECaC2), possibly TRPV5 (ECaC1), the intracellular calcium-binding protein calbindin-D9k, plasma membrane calcium ATPase (PMCA1b), and the sodium/calcium exchanger (NCX1), all of which are upregulated by active vitamin D through VDR-mediated transcriptional control[1][2]. The paracellular route is regulated by tight junction proteins such as claudins (notably claudin 2 and claudin 12), and modulators include dietary calcium, vitamin D, parathyroid hormone, and fibroblast growth factor 23 (FGF-23)[1][4]. Disruption of this process is implicated in various pathologies related to deficient or excessive calcium absorption. Calcium absorption in the small intestine is **not** a specific molecular drug target (e.g., not a single receptor, enzyme, or channel) but a complex, multi-component physiological process. For therapeutic targeting or molecular drug discovery, focus is typically placed on individual molecules such as *transient receptor potential cation channel subfamily V member 6 (TRPV6)*, *calbindin-D9k*, or the *vitamin D receptor (VDR)*, all of which are valid molecular drug targets involved in this process[1][2][4].

Other names

Intestinal calcium absorptiongut calcium absorption

Enhancement of transcellular and paracellular calcium transport by upregulating expression and function of calcium transporters/channels via vitamin D receptor (VDR)[1][2][4]