Researchers are shedding new light on how chronic inflammation contributes to fibrosis, an abnormal buildup of scar-like tissue in the aging heart, a process that can impair cardiac function and increase the risk of disease.

Fibrosis is a hallmark of aging, arising when the body’s standard tissue-maintenance systems begin to falter. Central to this decline are fibroblasts, the cells responsible for producing and regulating the heart’s extracellular matrix, the structural framework that helps maintain healthy cardiac function. As fibroblasts become dysregulated with age, they drive excessive matrix deposition, leading to stiffening and structural disruption of heart tissue.

Scientists report that persistent, low-grade inflammation in older tissues plays a major role in this shift. Inflammatory signals, common in aging, interfere with many cellular processes, including those governing fibroblast behavior. This creates a cascade of dysregulated activity that accelerates tissue remodeling and worsens cardiac decline.