Background/Objectives: Vitamin D is a crucial micronutrient involved in calcium homeostasis, bone metabolism, and various cellular signaling pathways. Recent evidence suggests that Transient Receptor Potential Canonical 6 (TRPC6), a calcium-permeable cation channel involved in intracellular calcium influx, may be influenced by hormonal regulation. This study aimed to investigate the relationship between vitamin D deficiency and circulating TRPC6 levels in a clinical population. Methods: A total of 100 patients diagnosed with vitamin D deficiency and 100 frequency-matched healthy controls were included in the study. Serum 25-hydroxyvitamin D [25(OH)D], calcium, potassium, and parathyroid hormone (PTH) levels were measured using standard biochemical methods, while serum TRPC6 concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Results: Demographic characteristics, including age, sex distribution, body weight, height, and body mass index, were comparable between the groups (p > 0.05). Serum TRPC6 levels were significantly higher in patients with vitamin D deficiency than in healthy controls (4.85 ± 2.49 vs. 4.33 ± 2.92 ng/mL, p = 0.0457). In contrast, no significant differences were observed between the groups regarding calcium (p = 0.6554), potassium (p = 0.1483), and PTH levels (p = 0.1234). Linear regression models revealed that continuous 25(OH)D levels were significant independent predictors of serum TRPC6 levels, and sex-stratified analyses further demonstrated distinct pattern dynamics between male and female cohorts. Conclusions: Vitamin D deficiency was associated with altered circulating TRPC6 levels independent of systemic calcium, potassium, and PTH homeostasis. The absence of significant differences in calcium and PTH concentrations suggests that TRPC6 alterations may represent an early molecular response to vitamin D deficiency before overt disturbances in mineral metabolism become evident. These findings provide novel evidence supporting a potential interaction between vitamin D status and TRPC6-mediated calcium signaling pathways and may contribute to a better understanding of the molecular mechanisms underlying bone metabolism. Further studies are required to clarify the biological significance of TRPC6 alterations and their potential role in osteoporosis and other bone-related disorders.
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Kargün et al. (2026) studied this question.
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