A photo of Satish Madala.

Associate Professor, UC Department of Pediatrics

513-636-9852

Biography & Affiliation

Biography

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.

Academic Affiliation

Associate Professor, UC Department of Pediatrics

Divisions

Pulmonary Medicine, Fibrosis



Blog Posts

Education

Postdoctoral training: Wynn Lab, Immunopathogenesis Section, LPD, NIAD, NIH, Bethesda, MD.

PhD: National Institute of Nutrition, Osmania University, Hyderabad, India.

Publications

Selected Publication

Wilms' tumor 1 drives fibroproliferation and myofibroblast transformation in severe fibrotic lung disease. Sontake, V; Kasam, RK; Sinner, D; Korfhagen, TR; Reddy, GB; White, ES; Jegga, AG; Madala, SK. JCI insight. 2018; 3.

Unsupervised gene expression analyses identify IPF-severity correlated signatures, associated genes and biomarkers. Wang, Y; Yella, J; Chen, J; McCormack, FX; Madala, SK; Jegga, AG. BMC Pulmonary Medicine. 2017; 17.

Repetitive intradermal bleomycin injections evoke T-helper cell 2 cytokine-driven pulmonary fibrosis. Singh, B; Kasam, RK; Sontake, V; Wynn, TA; Madala, SK. American Journal of Physiology: Lung Cellular and Molecular Physiology. 2017; 313:L796-L806.

Hsp90 regulation of fibroblast activation in pulmonary fibrosis. Sontake, V; Wang, Y; Kasam, RK; Sinner, D; Reddy, GB; Naren, AP; McCormack, FX; White, ES; Jegga, AG; Madala, SK. JCI insight. 2017; 2.

Unique and Redundant Functions of p70 Ribosomal S6 Kinase Isoforms Regulate Mesenchymal Cell Proliferation and Migration in Pulmonary Fibrosis. Madala, SK; Sontake, V; Edukulla, R; Davidson, CR; Schmidt, S; Hardie, WD. American Journal of Respiratory Cell and Molecular Biology. 2016; 55:792-803.

IL-31-Driven Skin Remodeling Involves Epidermal Cell Proliferation and Thickening That Lead to Impaired Skin-Barrier Function. Singh, B; Jegga, AG; Shanmukhappa, KS; Edukulla, R; Khurana, GH; Medvedovic, M; Dillon, SR; Madala, SK. PLoS ONE. 2016; 11:e0161877-e0161877.

Fibrocytes Regulate Wilms Tumor 1-Positive Cell Accumulation in Severe Fibrotic Lung Disease. Sontake, V; Shanmukhappa, SK; DiPasquale, BA; Reddy, GB; Medvedovic, M; Hardie, WD; White, ES; Madala, SK. Journal of immunology (Baltimore, Md. : 1950). 2015; 195:3978-3991.

Th2 Cytokines Augment IL-31/IL-31RA Interactions via STAT6-dependent IL-31RA Expression. Edukulla, R; Singh, B; Jegga, AG; Sontake, V; Dillon, SR; Madala, SK. The Journal of biological chemistry. 2015; 290:13510-13520.

Bone Marrow-Derived Stromal Cells Are Invasive and Hyperproliferative and Alter Transforming Growth Factor-alpha-Induced Pulmonary Fibrosis. Madala, SK; Edukulla, R; Schmidt, S; Davidson, C; Ikegami, M; Hardie, WD. American Journal of Respiratory Cell and Molecular Biology. 2014; 50:777-786.

Dual Targeting of MEK and PI3K Pathways Attenuates Established and Progressive Pulmonary Fibrosis. Madala, SK; Edukulla, R; Phatak, M; Schmidt, S; Davidson, C; Acciani, TH; Korfhagen, TR; Medvedovic, M; LeCras, TD; Wagner, K; et al. PLoS ONE. 2014; 9:e86536-e86536.