Elisabeth M. Zeisberg

TL;DR: It is shown that cardiac fibrosis is associated with the emergence of fibroblasts originating from endothelial cells, suggesting an endothelial-mesenchymal transition (EndMT) similar to events that occur during formation of the atrioventricular cushion in the embryonic heart.

TL;DR: It is shown that transforming growth factor-beta1 could induce proliferating endothelial cells to undergo a phenotypic conversion into fibroblast-like cells and EndMT is a unique mechanism for the accumulation of carcinoma-associated fibroblasts and suggested that antiangiogenic treatment of tumors may have a direct effect in decreasing activated fibro Blasts that likely facilitate cancer progression.

TL;DR: It is demonstrated that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT), and it is suggested that targeting EndMT might have therapeutic potential.

TL;DR: The function and origin of fibroblasts in cardiac fibrosis is reviewed and evidence is evolving that the cardiac fibroblast is a highly heterogenic cell population, and that such heterogeneity is caused by the distinct origins of Fibroblast in the heart.

TL;DR: It is demonstrated here that hypermethylation of RASAL1, encoding an inhibitor of the Ras oncoprotein, is associated with the perpetuation of fibroblast activation and fibrogenesis in the kidney.