Researchers from the University of Coimbra in Portugal identified a rise in the protein lactadherin within the coronary arteries that may signal the activation of inflammatory pathways tied to rapid heart aging. The findings were reported in the journal Molecular and Cellular Proteomics (MCP).
The investigation examined changes in heart muscle tissue in both mice and humans, focusing on the natural aging process and aging accelerated by various illnesses. The team observed that certain heart tissues, especially the extracellular matrix, undergo notable transformations as the heart’s function declines. The extracellular matrix serves as a support framework that helps maintain the structure of heart cells and surrounding vessels.
The remodeling of the extracellular matrix involves shifts in the levels of several proteins across heart and vascular tissues. Among these proteins, lactadherin was found to be produced in higher amounts during normal aging in older mice and humans, as well as in younger hearts facing accelerated aging due to disease. An elevated lactadherin concentration appears linked to the triggering of specific inflammatory signaling pathways that contribute to cardiovascular disease development.
Researchers also noted the potential for lactadherin-related mechanisms to align with broader questions about aging and neurodegenerative risk, suggesting new avenues for understanding how vascular changes might relate to diseases such as Alzheimer’s in some contexts. These observations warrant further study to determine how these pathways might be targeted for therapies aimed at slowing heart aging and reducing associated inflammation. The work adds to a growing body of evidence that protein changes in the heart’s supporting matrix play a central role in how aging unfolds at the tissue level. [Cited by research teams, with ongoing confirmation required in larger studies]