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Vitamin D is a prohormone that requires sequential enzymatic modification of 25 and 1a-hydroxylation in the liver and kidney respectively, leading to production of calcitriol (1,25(OH)2D3), the active form of vitamin D.1 Several studies have supported the notion that vitamin D, in addition to its classical action of maintaining systemic calcium homoeostasis and bone mineralisation, has non-classical extraskeletal actions including a potential capacity to inhibit fibrosis in various tissues. Murine lung fibroblasts treated with 1,25(OH)2D3, inhibited transforming growth factor (TGF)-β1-induced fibroblast proliferation, α-smooth-muscle actin expression, and diminished the upregulation of fibronectin and collagen expression. Furthermore, 1,25(OH)2D3 is able to inhibit the TGF-β1-dependent transdifferentiation of lung epithelial cells into myofibroblasts.2 Recent studies in mesenchymal multipotent cells showed that treatment with vitamin D led to an antiproliferative effect by inducing cell cycle arrest.3 Moreover, vitamin D reduced the collagen expression and other key profibrotic factors and increased the expression of antifibrotic factors, such as BMP7 and matrix metalloproteinase 8, in those cells.4 A mouse obstructed kidney model treated with paricalcitol (19-nor-1,25 hydroxyvitamin D2), a synthetic analogue of vitamin D, significantly …
Contributors SR and VN equally contributed to conception and drafting of the manuscript; and approval of the final version of the manuscript.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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