Calcium absorption promotion

"Calcium absorption promotion" refers to a broad set of molecular and physiological pathways that increase the uptake of calcium from the intestine into systemic circulation. The most critical effectors in this process are the vitamin D receptor (VDR; a nuclear hormone receptor), calcium channels such as TRPV6 (formerly CaT1), calbindin-D9k, and plasma membrane calcium ATPase (PMCA1b), all working together to facilitate active transcellular transport of calcium in the duodenum and upper jejunum. Paracellular (passive) mechanisms, regulated by tight-junction proteins like claudin-2, claudin-12, and claudin-15, also contribute, especially when calcium intake is high[1][2][3][4]. Endocrine factors such as vitamin D (via VDR), parathyroid hormone (PTH), prolactin, and calcitonin orchestrate these cellular changes to meet varying calcium demands in health and disease[3][4][5][6]. Because this description encapsulates a physiological process involving multiple distinct molecules and pathways, "calcium absorption promotion" is not considered a standalone druggable molecular target but instead a therapeutic goal enabled by modulating specific underlying molecular targets.

Other names

Calcium uptake enhancementenhanced intestinal calcium absorptionpromoted calcium transportstimulation of calcium uptake

Stimulation of active intestinal calcium transport (via upregulation of CaT1/TRPV6 and calbindin by 1,25-dihydroxyvitamin D3); Modulation of paracellular calcium absorption (via tight junction proteins such as claudin-2, claudin-12, claudin-15); Upregulation of calcium absorption by hormone signaling (e.g., vitamin D receptor, prolactin receptor)