A heart attack causes sudden loss of oxygen to the heart muscle, triggering cell death and a strong inflammatory response that often leads to scar formation. While scarring helps stabilize the heart, it reduces the heart’s ability to contract, forcing the remaining muscle to work harder and increasing the risk of heart failure. Existing drug-based strategies struggle to prevent this damage because treatments delivered through the bloodstream can affect the entire body and cause unwanted side effects. Now, a localized approach that directly supports healing in damaged heart tissue could help break this cycle and restore heart function.

Researchers at Texas A&M University (College Station, TX, USA) have developed a biodegradable microneedle patch that delivers a healing-promoting immune molecule directly into injured heart tissue. The patch is embedded with microscopic needles, each loaded with particles containing interleukin-4 (IL-4), a molecule known to regulate immune responses. When placed on the surface of the heart, the microneedles gently penetrate the outer layer of cardiac tissue and dissolve, releasing IL-4 precisely at the injury site without spreading throughout the body.

After a heart attack, immune cells called macrophages play a central role in determining whether inflammation worsens damage or supports repair. IL-4 shifts macrophages from a pro-inflammatory state to a healing state, reducing excessive scarring and encouraging tissue repair. By delivering IL-4 locally, the patch creates a regenerative environment that supports recovery while avoiding systemic immune effects seen with traditional injections.

In their study published in Cell Biomaterials, the researchers also observed changes in heart muscle cells following treatment. Cardiomyocytes became more responsive to signals from surrounding cells, particularly endothelial cells that line blood vessels. This enhanced cellular communication appears to support longer-term recovery by promoting healthier blood vessel function and improved coordination between cardiac cells.

In addition, the patch reduced inflammatory signaling from endothelial cells and increased activity in the NPR1 pathway, which plays an important role in maintaining blood vessel health and supporting overall heart function. These combined effects suggest the approach not only limits damage but also actively supports heart repair.

Although the current version of the patch requires open-chest surgery, the researchers are working toward minimally invasive delivery methods, such as catheter-based placement. Future refinements aim to make the therapy more practical for clinical use while preserving its targeted benefits.

“This is just the beginning,” said Texas A&M University researcher Dr. Ke Huang, who developed the patch. “We’ve proven the concept. Now we want to optimize the design and delivery.”

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