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Center of Excellence for Inflammation, Infectious Disease & Immunity

Quillen College of Medicine

Center News

CIIDI and Department of Surgery Graduate Student Presents at Annual Shock Conference

Xiaohui Wang, a graduate student in the Department of Surgery and the Center of Excellence in Inflammation, Infectious Disease and Immunity recently presented a research paper at the 38th Annual Conference on Shock.  Mr. Wang was awarded a Shock Society Travel grant to attend the meeting and present his findings. The Shock Society is an international scientific organization dedicated to facilitating integration of new techniques and research into the study of pathophysiology and the treatment of trauma, shock, and sepsis.

Wangs presentation, Toll-like Receptor 3 Stimulates Cardiomyocyte Proliferation and Cardiac Regeneration after Myocardial Infarction: Correlation with the Warburg Effect focused on his current research on Toll-Like Receptor 3 (TLR3) and its role in repairing heart cells (called cardiomocytes) after a heart attack.

If a patient survives a heart attack, the body tries to regenerate and repair the damaged heart cells.Cardiomyocyte form and function However, the adult heart losses the capability for the regeneration and repair of damaged heart tissue. The inflammatory responses and fibroblast proliferation will then create scar tissue in an attempt to repair the damaged heart. This scar tissue is irreversible and weakens the heart. It leaves the heart open to other major issues including future heart attacks and can eventually lead to heart failure. Heart failure is the leading cause of death globally.

Past research implies that heart cells are less likely to regenerate and repair themselves as the body ages. In striking contrast, very young subjects may have the capacity to fully repair heart tissue. Building on this knowledge, Wang observed, for the first time, that TLR3 is required for the regeneration and repair of the damaged heart. In very young mice, the heart is almost fully repaired after a heart attack. However, with the inhibition of TLR3, the very young mice lost the capacity for repair and regeneration of the damaged heart. The lack of TLR3 essentially starves the heart cells responsible for regeneration and repair. This stops the heart from repairing itself properly after trauma.

Healthy TLR3

Additionally, adult mice treated with a TLR3 ligand had an increase in healthy heart cells responsible for regeneration and repair. This work demonstrated the importance of TLR3 in heart cell regeneration and repair and could eventually pave the way for treatments for recovering cardiac patients.

Wang stated that these findings were somewhat surprising. Research on TLR3 has mainly focused on immune responses but this project was especially interesting because it also involved heart regeneration and repair. I love research, Wang said. I am very interested in continuing to do this work.

 

 

 

 

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