New faculty members recently joined Penn State College of Medicine’s Department of Cellular and Molecular Physiology.
Kathryn Aird joined the department Nov. 28, 2016. She is an assistant professor and earned her PhD from Duke University in 2010 and completed postdoctoral fellowship at The Wistar Institute from 2010 to 2016.
At Penn State College of Medicine, Aird’s lab studies the mechanisms and pathological implications of cellular senescence. Cellular senescence is a stable cell cycle arrest that is a bona vide tumor suppression mechanism and also plays a role in age-related pathologies. In particular, her lab is interested in the intersection between cellular senescence and metabolism. Understanding the mechanisms of how cells undergo and overcome this proliferative arrest may lead to novel therapeutic strategies for both cancer and aging. The lab mainly focuses on ovarian cells as a model system. Her lab aims to both understand the earliest events in ovarian tumorigenesis, and exploit senescence and metabolic pathways as novel therapeutic strategies for ovarian cancer patients. The Aird lab is currently funded by a R00 Award from the NIH/NCI.
Kebin Hu joined the department Jan. 9, 2017. He is an associate professor and earned his MD and his PhD from Nanjing University School of Medicine in Nanjing, China, in 1997 and 2001 respectively.
At the College of Medicine, Hu’s laboratory is interested in understanding the cellular and molecular mechanisms of tissue fibrogenesis and inflammation, identifying novel signal mediators, and developing therapeutic strategies for the treatment of fibrotic or inflammatory diseases.
The hallmark of chronic kidney disease (CKD) is renal interstitial fibrosis and inflammation, which is characterized by proliferation and activation of interstitial cells, florid infiltrations, extensive deposition of extracellular matrix (ECM) components, and the eventual destruction of normal kidney structure. Members of plasminogen activator system including tissue-type plasminogen activator (tPA) are the key regulators in the homeostasis of ECM. In addition to its protease activities, the Hu lab demonstrated that tPA is actually a cytokine promoting renal fibrosis and inflammation through its receptors-mediated activation of different cascades of intracellular signal transduction.
With the support of grants from NIH, American Heart Association, as well as other foundations, the laboratory is currently utilizing integral in vivo and in vitro approaches to define novel signal pathways in the regulation of fibroblast or macrophage differentiation and transdifferentiation and their roles in tissue fibrosis and inflammation, and to explore novel therapeutic remedies to retard or even reverse the progression of CKD.
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