Inflammaging and Senescence-Driven Extracellular Matrix Remodeling in Age-Associated Cardiovascular Disease.
As we age, our cardiovascular system undergoes changes that can unfortunately lead to heart disease. New insights point to two major culprits behind these age-related issues: “inflammaging” and “cellular senescence.”
Inflammaging is essentially a persistent, low-level inflammation that gradually harms our tissues as we get older. Alongside this, “cellular senescence” occurs when cells stop dividing and, instead, start releasing a mix of inflammatory signals and other damaging substances—a process called the “senescence-associated secretory phenotype” (SASP). These senescent cells build up in our bodies, acting like troublemakers that contribute to aging.
Working together, inflammaging and senescent cells cause unhealthy alterations in the “extracellular matrix,” which is the vital support structure surrounding our cells and tissues. This “maladaptive extracellular matrix remodeling” can lead to stiffening of blood vessels and impaired “endothelial function,” meaning the inner lining of our blood vessels can no longer work properly to regulate blood flow and prevent clotting. Ultimately, these changes weaken the integrity of our heart and blood vessels and promote “fibrosis,” which is the thickening and scarring of tissue.
By understanding these fundamental processes, scientists are developing new ways to combat age-related heart conditions. Promising strategies include “senolytics”—drugs designed to selectively remove harmful senescent cells—as well as treatments aimed at reducing inflammation or restoring the healthy structure of the extracellular matrix. These advancements offer hope for future therapies to prevent and treat cardiovascular diseases in older adults.