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Madala lab research goals are to identify the cellular and molecular mechanisms underlying chronic lung remodeling diseases and develop new therapies. Fibrosis is the deposition of collagen and other extracellular matrix (ECM) proteins in tissues, a pathology common to many Interstitial Lung Diseases including Idiopathic Pulmonary Fibrosis (IPF). Fibrosis in the lung disrupts gas exchange in the alveoli of the lungs. It is the leading cause of morbidity and mortality in respiratory diseases. Despite this disease’s enormous impact on human health, there are no approved treatments that directly target the mechanism(s) of fibrosis. Our research on genomic comparisons of IPF and non-IPF cells revealed significant differences in the cellular and molecular pathways of IPF cells. We were the first to describe an increase of WT1 and Sox9 protein in IPF and the first to show that this dysfunction significantly increased fibroblast activation and ECM production. Using advanced cell lineage tracing methods, we showed in vivo that WT1-positive mesothelial cells transform into mesenchymal cells in the pathogenesis of pulmonary fibrosis. The primary focus of our ongoing research efforts is to advance our use and understanding of fibroblast activation which leads to novel therapeutic approaches in the treatment of severe fibrotic lung diseases.
The lab has developed novel in vitro and in vivo models to study severe fibrotic lung diseases such as IPF and other ILDs. Using a combination of experimental, technological, and computational approaches, we like to probe and elucidate the cellular and signaling processes that maintain persistent fibrosis in the lung. The laboratory also studies calcium signaling and contractile mechanisms of airway smooth muscle cells in asthma and other chronic lung diseases.
The key findings of my laboratory include:
University of CincinnatiDepartment of Internal Medicine Division of Pulmonary, Critical Care, and Sleep Medicine 231 Albert Sabin Way, ML 0564 Cincinnati, OH 45267-0564
Phone: 513-558-4831 Fax: 513-558-4858 Email: pulmonary@uc.edu