Scientists Are Reversing Heart Disease at the Cellular Level—Here's What That Means for You

Cardiovascular disease has been America's leading cause of death for over a century, but researchers are now uncovering ways to reverse the cellular damage that causes it. At Florida International University (FIU), biomedical engineers and physician-scientists are investigating the earliest stages of heart disease—before symptoms even appear—and developing treatments that could make plaque disappear entirely, not just slow its growth.

Why Does Heart Disease Develop in Some People but Not Others?

Your heart beats roughly 100,000 times per day, contracting and relaxing in a precise rhythm that keeps oxygen-rich blood flowing through your arteries and veins. For some people, this system works flawlessly for an entire lifetime. For others, something goes wrong—and often, they don't realize it until significant damage has already occurred. "By the time symptoms appear, the heart has been irreparably damaged," explains Joshua Hutcheson, a biomedical engineer and Fellow of the American Heart Association who leads the Cardiovascular Matrix Remodeling Lab at FIU.

The culprit is often atherosclerosis, a silent process where plaque builds up inside artery walls. This buildup can begin as early as childhood and progresses over decades without causing any noticeable symptoms. The plaque consists of cholesterol, inflammatory cells, and other materials that gradually narrow the artery, reducing blood flow. The real danger comes when this plaque becomes unstable and ruptures, triggering blood clots that can block blood flow entirely—causing a heart attack.

What's Driving the Surge in Heart Disease Cases?

The American Heart Association estimates that at least six in 10 U.S. adults—more than 184 million people—will have some type of cardiovascular disease by 2050. This projection reflects a troubling collision course: while death rates from heart disease have declined over recent decades thanks to blood pressure medications, cholesterol-lowering drugs, and smoking cessation campaigns, that downward trend is now stalling. An aging population is expected to drive a surge in cardiovascular disease cases, while simultaneously, a growing number of younger adults are developing risk factors such as uncontrolled blood pressure, diabetes, and obesity.

How Are Scientists Stopping Plaque Formation at the Cellular Level?

Hutcheson's breakthrough research focuses on the earliest mechanisms of arterial calcification—the process where calcium deposits harden plaque. Working with colleagues at Harvard, he discovered that tiny membrane sacs called extracellular vesicles are the primary drivers of this calcification process. These nanosized bubbles bleb off from cells, cluster together, and begin "capturing" calcium and phosphate, essentially kickstarting the plaque formation process.

Once Hutcheson identified these vesicles as the culprits, his team tested whether existing medications could stop them. The results were encouraging: epidermal growth factor receptor inhibitors—drugs already approved by the FDA for cancer treatment—successfully prevented the vesicles from triggering plaque formation in cell culture experiments. This discovery opens the possibility of repurposing existing medications to prevent heart disease before it starts.

But prevention is only part of the equation. Hutcheson's research group has also made progress on what many consider the ultimate goal: reversing existing plaque. In preclinical mouse models and human cells, activating a hormone called relaxin using a small molecule developed with the National Center for Advancing Translational Sciences significantly reduced and reversed late-stage vascular calcification. "This is the dream," Hutcheson says. "To find a way to reverse the pathology and return patients to a normal baseline."

Current treatments like cholesterol-lowering drugs and lifestyle changes typically slow the formation of new plaque but don't eliminate existing buildup. The potential to actually reverse calcification represents a fundamental shift in how we could treat heart disease.

What Other Heart Innovations Are in Development?

Beyond arterial plaque, researchers at FIU are tackling another critical component of heart health: the heart valves. These one-way doors open and close with each heartbeat, creating the "lub-dub" sound you hear through a stethoscope. When valves don't function properly—either failing to open fully or closing incompletely—blood flow becomes compromised. Researchers in Hutcheson's lab are investigating new solutions to valve dysfunction, though the full scope of these innovations extends beyond the current research focus.

The convergence of these discoveries suggests a future where cardiovascular disease could be detected and treated at much earlier stages. By understanding the cellular mechanisms that drive plaque formation and calcification, researchers are moving beyond managing symptoms toward actually preventing and reversing the underlying disease process.

• Extracellular Vesicles: Tiny membrane sacs that trigger calcium and phosphate accumulation in arteries, identified as the primary drivers of arterial calcification and plaque formation.
• FDA-Approved Cancer Drugs: Epidermal growth factor receptor inhibitors successfully stopped vesicle-mediated plaque formation in laboratory experiments, offering a potential repurposing opportunity.
• Relaxin Hormone Activation: A small molecule that activates relaxin demonstrated the ability to significantly reduce and reverse late-stage vascular calcification in preclinical models and human cells.
• Calcification Paradox Research: Investigations into why abnormal arterial calcification correlates with reduced bone mineralization, potentially revealing ways to redirect calcium from arteries back into bone.

The implications of this research extend far beyond the laboratory. With cardiovascular disease projected to affect more than 184 million Americans by 2050, developing treatments that can reverse existing damage—rather than simply slowing progression—could transform outcomes for millions of people. The work at FIU represents a fundamental shift in how the medical community approaches one of humanity's oldest and most persistent health challenges.