S
Satish K. Madala
Researcher at Cincinnati Children's Hospital Medical Center
Publications - 50
Citations - 2293
Satish K. Madala is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Fibrosis & Pulmonary fibrosis. The author has an hindex of 21, co-authored 40 publications receiving 1926 citations. Previous affiliations of Satish K. Madala include University of Cincinnati Academic Health Center & National Institutes of Health.
Papers
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Journal ArticleDOI
Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent
Mark S. Wilson,Satish K. Madala,Thirumalai R. Ramalingam,Bernadette R. Gochuico,Ivan O. Rosas,Allen W. Cheever,Thomas A. Wynn +6 more
TL;DR: It is demonstrated that fibrosis induced by IL-1β, which mimics BLM-induced fibrosis, is also highly dependent on IL- 17A, illustrating the potential utility of targeting IL-17A in the treatment of drug and inflammation- induced fibrosis.
Journal ArticleDOI
Bone marrow stromal cells use TGF-β to suppress allergic responses in a mouse model of ragweed-induced asthma
Krisztián Németh,Andrea Keane-Myers,Jared M. Brown,Dean D. Metcalfe,James D. Gorham,Virgilio Bundoc,Marcus G. Hodges,Ivett Jelinek,Satish K. Madala,Sarolta Kárpáti,Eva Mezey +10 more
TL;DR: The results suggest that, in addition to focusing on graft-versus-host disease and autoimmune diseases, allergic conditions—specifically therapy resistant asthma—might also be a likely target of the recently discovered cellular therapy approach using BMSCs.
Journal ArticleDOI
Matrix Metalloproteinase 12-Deficiency Augments Extracellular Matrix Degrading Metalloproteinases and Attenuates IL-13–Dependent Fibrosis
Satish K. Madala,John T. Pesce,Thirumalai R. Ramalingam,Mark S. Wilson,Samantha Minnicozzi,Allen W. Cheever,Robert W. Thompson,Margaret M. Mentink-Kane,Thomas A. Wynn +8 more
TL;DR: Surprisingly, the reduction in liver and lung fibrosis in MMP12-deficient mice was not associated with significant changes in cytokine, chemokine, TGF-β1, or tissue inhibitors of matrix metalloproteinase expression, suggesting that Mmp12 was promoting fibrosis by limiting the expression of specific ECM-degrading MMPs.
Journal ArticleDOI
MEK-ERK pathway modulation ameliorates pulmonary fibrosis associated with epidermal growth factor receptor activation.
Satish K. Madala,Stephanie Schmidt,Cynthia Davidson,Machiko Ikegami,Susan E. Wert,William D. Hardie +5 more
TL;DR: It is demonstrated that MEK inhibition prevents progression of established fibrosis in the TGF-α model, and provides proof of concept of targeting the MEK pathway in fibrotic lung disease.
Journal ArticleDOI
Mechanisms of Lung Fibrosis Resolution
Stephan W. Glasser,James S. Hagood,Simon S. Wong,Carmen A. Taype,Satish K. Madala,William D. Hardie +5 more
TL;DR: This review describes the current understanding of the mechanisms whereby the lung is known to resolve fibrosis focusing on degradation of the extracellular matrix, removal of myofibroblasts, and the role of inflammatory cells.