Aims: The main cellular source of extracellular matrix (ECM) in the fibrotic liver are myofibroblast-like cells (MFB) originating from mesenchymal hepatic stellate cells (HSC). In the fibrotic processes of kidney (mesangial cells), heart (cardiac fibroblasts) and dermis (dermal fibroblasts) it has been shown that the accessory receptor endoglin is upregulated in the respective profibrogenic cells and modulates fibrosis relevant responses mediated by TGF-β1 [1–3]. In activated HSC, endoglin is also highly expressed but its functional relevance in TGF-β1-signaling has not been determined [4].
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