A recent study led by Virginia Tech has achieved a breakthrough. Scientists have discovered that a molecule called connexin 43 plays an essential role in the repair process following damage to the inner walls of blood vessels. This discovery brings new hope for improving the long-term success rate of coronary artery stenting and bypass surgery.

Statistics show that nearly 600,000 patients in the United States undergo these cardiovascular surgeries each year. Despite continuous advancements in surgical techniques, restenosis remains a major cause of treatment failure. The root of the problem often lies in the inevitable damage that surgical instruments can inflict on the vascular endothelium—a delicate barrier lining the inside of blood vessels, only a single cell thick. The integrity of this cellular layer directly affects the quality of wound healing and the long-term patency of blood vessels.

The study's lead author, Assistant Professor Scott Johnstone of the Fralin Institute for Biomedical Research, explained that both the compression caused by the stent opening the blood vessel and the handling of the vein graft during bypass surgery can damage or slough off endothelial cells. If the endothelium cannot regenerate effectively, it will trigger a series of chain reactions, potentially leading to re-blockage of the blood vessel.

The research team focused on connexin 43. This protein is known to construct intercellular communication channels and has been studied in skin healing, but its specific role in vascular endothelial repair remains unknown. Through sequencing analysis of tens of thousands of single-cell vascular structures from mice, the team observed that endothelial cells rapidly upregulate connexin 43 expression after vascular injury. When the function of this protein was inhibited using gene technology, the repair rate of the vascular endothelium was significantly delayed, confirming its crucial role in the healing process.

Professor Johnstone emphasized that this study is the first to depict a core pathway for endothelial injury repair within a complete living system. Its significance lies not only in revealing a new therapeutic target—potentially enabling the development of drugs to enhance this repair mechanism—but also in providing important references for the safety assessment of existing drugs, helping to avoid drug interference with the normal healing process.

The findings have been published in *Heart and Circulatory Physiology*, a leading journal in the field of physiology. The research was funded by the American Heart Association, the National Institutes of Health, and other institutions. The research team stated that their next step will be to further explore how to safely and effectively modulate this pathway, thereby promoting cardiovascular surgery from success to lasting rehabilitation.

Journal Source:

Sedovy, MW, et al. (2025). Injury-induced Connexin 43 expression regulates endothelial cell wound healing. American Journal of Physiology-Heart and Circulatory Physiology . DOI: 10.1152/ajpheart.00153.2025.