The Myocarditis Foundation is pleased to announce that it will be funding a research fellowship grant for the 2016/2017 grant cycle. The Myocarditis Foundation will be awarding the research grant to Dr. Jon Sin of Cedars-Sinai Medical Center in the amount of $40,000. Dr. Sin is under the mentorship of Dr. Ralph Feuer of Cedars-Sinai Medical Center.

Jon Sin

The Myocarditis Foundation, an international non-profit organization founded in 2005, is dedicated to increasing awareness and hastening progress in understanding this rare disease. Myocarditis is a disease that is marked by inflammation and scarring of the heart muscle, which can progress rapidly to heart failure and death or heart transplantation.

The Myocarditis Foundation announced in its third quarter of 2015 that it was accepting grant applications until December 1, 2015. The Myocarditis Foundations International Medical Advisory Board, made up of leading myocarditis researchers from around the world, voted to award a fellowship grant to Dr. Sin after selecting his application from a distinguished field of candidates.

Dr. Sins research project is titled Coxsackievirus B Subverts Host Mitophagy to Promote Viral Dissemination and Myocarditis. Below is a laymans summary of his research:

Coxsackievirus B (CVB) is a common juvenile pathogen that can cause a wide-array of inflammatory diseases including meningitis, pancreatitis, and myocarditis, all of which can be fatal. We see that CVB, which is a naked virus, can escape the cell in membrane-bound vesicles which we hypothesize are derived from autophagosomes. Not only does this blur the line between enveloped and non-enveloped viruses, but it also suggests that CVB could use these host membranes to evade the immune system. Additionally when we infect cardiomyocytes, mitochondrial networks appear to fragment, which is an early step in the autophagic degradation of mitochondria (mitophagy). Normally, these fragmented mitochondria would be targeted for destruction; however we find that in the setting of infection, mitochondrial fragments and virus are ejected from the cell in membrane-bound vesicles. If we pharmacologically block mitochondrial fission prior to infection, this results in lower viral titers in the media and fewer infected cells, suggesting that blocking the early steps in mitophagy suppresses viral escape. We hypothesize that the virus triggers mitochondrial fission and uses these fragments as bait in order to become encapsulated in autophagosomes and get ejected from the cell in order to further spread infection. Based on our preliminary findings, we are now utilizing a mouse model of CVB infection to test the efficacy of using a mitochondrial fission inhibitor to suppress vital myocarditis.

-Summary by Dr. Sin

The Myocarditis Foundation is honored to work with Dr. Sin and the Cedars-Sinai Medical Center, furthering the expansion of myocarditis research. It is the Foundations goal to build a greater understanding of the disease and find better ways to diagnose, treat and ultimately prevent myocarditis from taking more lives.

The Myocarditis Foundation would like to thank all the families, businesses, and organizations that have supported the Foundation in 2015. It is with their generosity and support that these research grants are able to be awarded each year.

For more information regarding the Myocarditis Foundation and its grant program, please visit, myocarditis.viewsamplesite.com.

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