Tien Peng, MD
|School||UCSF School of Medicine|
|Address||533 Parnassus Ave, UC Hall|
San Francisco CA 94143
|University of Virginia||B.A.||2000|
|Johns Hopkins University||M.D.||School of Medicine||2006|
|National Institutes of Health||2003
||2004||Clinical Research Training Program Scholar|
|University of Pennsylvania||2013
||2014||Willam Maul Measey Senior Research Fellow|
|University of Pennsylvania||2013||Stanley E. Bradley Award for Bench Research|
|Federation of American Societies for Experimental Biology||2014||Jo Rae Wright Award|
Tien Peng received his BA from the University of Virginia in 2000 and MD from Johns Hopkins University in 2006. He trained in Internal Medicine at Columbia University Medical Center and Pulmonary and Critical Care Medicine at the Hospital of the University of Pennsylvania. He completed his postdoctoral research training in the Department of Cell and Developmental Biology at the University of Pennsylvania.
My laboratory is interested in studying how key developmental pathways continue to persist in adulthood to maintain normal homeostatic organ function. We are particularly focused on the mesenchymal cell types (e.g. fibroblasts) that are poorly understood and lack precise anatomical definition, but are integral to the structural integrity and function of adult organs such as the lung. My postdoctoral work focused on how the Hedgehog pathway directed mesenchymal progenitor differentiation during embryonic development, and much to our surprise, how Hedgehog continues to maintain normal mesenchymal homeostasis during adulthood. We found that cellular quiescence in the adult lung is not a default state, but rather actively maintained by epithelial-mesenchymal crosstalk coordinated by Hedgehog. This suggests that cellular quiescence is tightly regulated by the state of Hedgehog activation within the mesenchyme to regulate cellular turnover during homeostasis and injury, and that dysregulated Hedgehog signaling could lead to maladaptive remodeling and lung diseases. My lab is studying the mechanisms underlying the maintenance of cellular quiescence, and how dysregulated quiescence could lead to disease states.
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