Mark Renton grew up in Australia playing football as soon as he could. He imagined a future career helping athletes with strength training and exercise plans.
But during his undergraduate studies, a course on exercise metabolism changed his focus. The class looked at how cells convert energy into movement. This sparked Renton’s interest in how muscles work, especially how they generate force through precise contractions. This curiosity eventually led him to pursue a doctorate studying the heart—the body’s most important muscle.
Now at the Fralin Biomedical Research Institute at VTC, Renton continues his heart research with support from a postdoctoral fellowship awarded by the American Heart Association. His study focuses on coronary microvascular dysfunction.
Most people associate heart disease with heart attacks. However, problems in the heart’s smaller blood vessels can develop long before any chest pain appears. In coronary microvascular disease, damaged vessels reduce blood flow to the heart. Obesity is one condition that greatly increases this risk.
With his fellowship funding, Renton will study a protein called pannexin-1. He believes this protein may explain how obesity affects heart health. “Pannexin-1 is a channel,” Renton explained. “It sits on the outside of the cell membrane and lets ions move in and out of the cell and between neighboring cells. These ions start signals inside the cell that tell it what to do.”
The connection between obesity and heart disease is well known. Recently, Renton’s lab, led by Scott Johnstone, found that removing pannexin-1 causes blood vessels in the heart to lose their ability to expand and contract properly. This same problem happens in obesity.
When the blood vessels lose this function, they can spasm and cause chest pain. Renton’s goal is to discover whether obesity causes this loss by reducing the number of pannexin-1 channels, changing how they work, or altering the signals they send.
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