My research interests include idiopathic pulmonary fibrosis, asthma, scleroderma, cystic fibrosis and lung injury. My goal is to identify the cellular and molecular mechanisms underlying chronic lung diseases to guide the development of new therapies.
Fibrosis is the deposition of collagen and other extracellular matrix (ECM) proteins in tissues, a pathology common to many severe and chronic diseases. 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. My research seeks to identify the cellular source and control mechanisms that result in the initiation and progression of pulmonary fibrosis. These studies will provide evidence for the development of novel therapeutic targets to treat fibrosis.
My research covers three major lung diseases: idiopathic pulmonary fibrosis (IPF), asthma and cystic fibrosis. The key findings of my laboratory include:
- Identifying mesenchymal cell subsets, signaling pathways and molecules involved in pulmonary fibrosis (Journal of Immunology 2010, 2015; American Journal of Respiratory Cell and Molecular Biology 2014, 2016; JCI Insight 2018)
- Identifying novel therapeutic targets and develop new therapies to reverse established and ongoing pulmonary fibrosis (American Journal of Respiratory Cell and Molecular Biology 2012, 2014; American Journal of Physiology Lung Cellular and Molecular Physiology 2014, 2016, 2017; JCI Insight 2017; EMBO Mol. Med. 2020)
- Identified downstream mediators of Th2 T cells involved in tissue remodeling and lung function decline (Journal of Biological Chemistry 2019, 2015; PLOS One 2016)
Our research on genomic comparisons of IPF and non-IPF cells revealed significant differences in cellular and molecular pathways of IPF cells. We were the first to describe an increase of WT1 protein in IPF and the first to show that this dysfunction resulted in a significant increase in fibroblast activation and ECM production. Using advanced cell lineage tracing methods, we showed in vivo that WT1-positive mesothelial cells transform to mesenchymal cells in the pathogenesis of pulmonary fibrosis.
I am honored to have received many awards throughout my career, including:
- The Parker B. Francis Jo Rae Wright Award for Scientific Excellence, USA (2019)
- Best Poster Award, FASEB Conference, Olean, NY, USA (2018)
- Science and Innovation Center (SIC) Rising Star Research Award, Respiratory Cell & Molecular Biology (RCMB) Assembly, American Thoracic Society (ATS), Washington, DC, USA (2017)
- Best Abstract Award, Gordon Conference on Lung Injury and Repair, Andover, NH, USA (2015)
- Parker B. Francis (PBF) Fellow Award, PBF Foundation, USA (2013)
- Young Investigator Award, International Summit on Fibrosis, Cleveland Clinic, USA (2010)
- Best Abstract Award, Fibrosis Meeting, Keystone Symposia, Keystone, CO, USA (2009)
- Fellows Award for Research Excellence (FARE), Excellence in Biomedical Research, NIH, Bethesda, USA (2008)
- Dr. K. V. Rao Annual Research Award, India (2004)
- Council of Scientific and Industrial Research-University Grants Commission (CSIR-UGC) Fellowship, Government of India (2000)
The primary focus of our ongoing research efforts is to advance our use and understanding of genomics in preclinical modeling that leads to novel therapeutic approaches in the treatment of chronic lung diseases.
Associate Professor, UC Department of Pediatrics
Pulmonary Medicine, Fibrosis