Abstract
My research experience in the field of scleroderma began in year 2000 when I was recruited as a postdoctoral fellow to the laboratory of Dr. Richard M. Silver. Since that time my research interests has focused on understanding the cellular and molecular mechanisms of pulmonary fibrosis in scleroderma patients.
Highlights
My research experience in the field of scleroderma began in year 2000 when I was recruited as a postdoctoral fellow to the laboratory of Dr Richard M
The ongoing research in the laboratory can be subdivided in three major projects: The first is thrombin signaling in scleroderma lung disease, the second is CTGFinteracting proteins in scleroderma-associated pulmonary fibrosis, and the third project concentrates on the role of genome in scleroderma
We observed that dabigatran etexilate significantly reduced thrombin activity and levels of TGF-β1 in Broncho alveolar Lavage Fluid (BALF), while simultaneously decreasing inflammatory cells and protein concentrations in BALF [15]
Summary
My research experience in the field of scleroderma began in year 2000 when I was recruited as a postdoctoral fellow to the laboratory of Dr Richard M. Activation of these cells by thrombin is a likely mechanism for the development and progression of pulmonary fibrosis in general, and SSc-ILD in particular. Our laboratory as well as others has demonstrated dramatically increased levels of thrombin in Broncho alveolar Lavage Fluid (BALF) from scleroderma patients with lung fibrosis and other fibrosing lung diseases [4,5].
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