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Qiongxin Wang, MD, PhD

Phone314-362-1291

Education

  • Bachelor's in Medicine: Tongji Medical College, Huazhong University of Science and Technology, Hubei, China (2005)
  • Master's in Internal Medicine: Tongji Medical College, Huazhong University of Science and Technology, Hubei, China (2008)
  • Research Scholar: The University of Oklahoma Health Sciences Center, Oklahoma City, Ok (2010)
  • MD & Phd in Internal Medicine: Tongji Medical College, Huazhong University of Science and Technology, Hubei, China (2012)
  • Postdoctoral fellow: The University of Oklahoma Health Sciences Center, Oklahoma City, Ok (2012)
  • Assistant Staff Scientist: Oklahoma Medical Research Foundation, Oklahoma (2015)
  • Senior Postdoctoral fellow: The University of Oklahoma Health Sciences Center, Oklahoma City, OK (2016)
  • Senior Postdoctoral fellow: The University of Alabama at Birmingham, AL (2017)
  • Scientist 1: The University of Alabama at Birmingham, AL (2020)

Research Interests

I have been working on the development of an entirely new scientific paradigm for the basis of cardiac inflammation in heart failure, one that ascribes a key role to specific immune cells in ischemic cardiomyopathy. The explicit profiles of macrophage subsets and according capacities have been built on our mouse models with acute and chronic heart failure. Specifically, my work has found that macrophages in the failing heart expressing the protein CD206 and a subunit of the receptor for interleukin-4 (IL-4Ra) are important disease drivers. CD206+IL-4Ra+ macrophages proliferate and expand in the failing heart and are key drivers of pathological remodeling and fibrosis, in part through the secretion of FIZZ1. Moreover, therapeutically targeting these CD206+IL-4Ra+ macrophages has represented an effective approach to alleviating cardiac inflammation and heart failure in mice in vivo. Our ongoing studies are decoding the genomic characterizations of CD206+IL-4Ra+ macrophages in rodent and human that will help better understand the underlying mechanisms of CD206+IL-4Ra+ macrophage-modulated heart failure and initiate novel therapeutic strategies for chronic heart failure.

 

Beyond the work on CD206+IL-4Ra+ macrophages in heart failure, I am expanding research to examine the role of other macrophage populations in the failing heart (such as CD206+ IL-10Rα+ macrophages) and the mechanisms by which these immune cells inflict damage and induce fibrosis (scar formation) in the heart. While this work is of direct importance to heart failure after a myocardial infarction, it also has direct relevance to other forms of heart injury. The loss of CD206+ IL-10Rα+ macrophages significant increases mortality of acute heart failure in mice with myocardial infarction due to the incapacity of scar formation and heart rupture This has indicated a dispensable role of CD206+ IL-10Rα+ macrophages in acute myocardial infarction. However, the importance of this macrophage subsets in the chronically failing and remodeled heart is completely unknown. Our future work is identifying the intricate effects of CD206+ IL-10Rα+ macrophages in chronic ischemic heart failure.

Publications

View publications on PubMed.gov