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Sodium-dependent phosphate transporter 1, commonly known as PiT1 or SLC20A1, is a transmembrane protein that functions as a high-affinity, sodium-dependent symporter for inorganic phosphate [1, 10]. It is ubiquitously expressed and plays a vital role in maintaining cellular phosphate homeostasis, which is essential for metabolism, signal transduction, and the synthesis of nucleic acids and lipids [2, 11]. Beyond its transport function, PiT1 is involved in regulating cell proliferation, TNF-induced apoptosis, and insulin signaling [3, 5]. In clinical contexts, PiT1 is a key driver of pathological vascular calcification, particularly in patients with chronic kidney disease or diabetes, as its upregulation promotes the osteogenic transdifferentiation of vascular smooth muscle cells [6, 12, 16]. It also serves as a receptor for the gibbon ape leukemia virus and has been linked to the progression of several cancers, including breast and pituitary adenomas [2, 5]. Therapeutic strategies targeting PiT1, such as the use of the inhibitor phosphonoformic acid (foscarnet), aim to prevent cardiovascular mineralization, although systemic safety concerns regarding phosphate balance and liver function must be addressed [6, 12, 13].
Competitive inhibition of sodium-dependent inorganic phosphate transport across the plasma membrane
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