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It is shown that MGP deficiency attenuates renal fibrosis, suppresses fibroblast activation, and preserves kidney function following folic acid nephropathy and unilateral ureteral obstruction, supporting MGP as a potential fibroblast-associated target for future strategies aimed at limiting CKD progression.
It is shown that SMOC2 localized to the basement membrane of injured TECs across 3 murine models of kidney injury and induced a partial epithelial-to-mesenchymal (EMT) transition in TECs, and its extracellular calcium-binding domain mediated binding to the decellularized extracellular matrix accounted for most of its e...
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