Associate Professor of Pharmaceutical Sciences at the University of Texas, Dr. Ke Huang, has developed a novel method for delivering therapeutic agents to heart tissues affected by pathological changes. This involves a biodegradable patch equipped with microscopic needles. Inside each needle are nanoparticles containing interleukin-4 (IL-4), a molecule known for its ability to modulate the immune response. The patch is attached to the surface of the heart; the needles dissolve, releasing IL-4 precisely into the damaged area, thereby creating favorable conditions for regeneration. The results of this study were published in the scientific journal Cell Biomaterials. The consequences of myocardial infarction include deficits in oxygen and nutrients, leading to cardiomyocyte death. Scar tissue forms in place of the dead cells, providing mechanical stability to the organ, but lacking the contractile ability characteristic of healthy muscle mass. Consequently, the heart must compensate for the lost function, which can eventually lead to the development of chronic heart failure. The main goal of this patch is to interrupt this pathological cascade. By delivering IL-4 directly to the ischemia zone, the patch initiates the switching of immune cells—macrophages—from a pro-inflammatory phenotype to a tissue-repair promoting phenotype. Such a transformation helps minimize fibrosis formation and, consequently, improves the long-term clinical prognosis. Previous approaches to using IL-4 involved its systemic administration into the bloodstream, which often caused off-target side effects in other organs. The patch proposed by Huang solves this problem by ensuring strictly localized action. A notable discovery was the change in cardiomyocyte behavior after treatment: Huang observed that the cells exhibited increased “interconnectedness” and better responsiveness to neighboring tissue signals, particularly signals from endothelial cells lining the vessels. This, in turn, could be crucial for long-term functional regeneration. Furthermore, the application of the patch led to a decrease in inflammatory mediators released by endothelial cells, which could exacerbate the condition following an acute infarction. Huang’s research team recorded the activation of a signaling pathway called NPR1, which is considered important for maintaining cardiac muscle and vascular system homeostasis. Currently, installing the patch requires an open-heart surgery procedure, and Dr. Huang is working on adapting the technology for less invasive methods. His plans include creating a version that could be delivered via catheter, which would significantly simplify its use in clinical practice.
About the Author
