Cellular Senescence As A Core Mechanistic Link Between CKD, Cardiac Fibrosis, And Aging
As we age, our bodies undergo various changes, and sometimes, cells can enter a state called “cellular senescence.” These are cells that have stopped dividing but remain active, and they can accumulate in tissues. Recent research highlights that this accumulation of senescent cells plays a crucial role in linking chronic kidney disease (CKD), the scarring of heart tissue (cardiac fibrosis), and the overall aging process.
When cells become senescent, they release a cocktail of inflammatory and pro-scarring molecules, collectively known as the senescence-associated secretory phenotype (SASP). This SASP creates a harmful environment that promotes inflammation, leads to the formation of scar tissue (fibrosis), and causes tissues to stiffen in both the kidneys and the heart. This means that these “retired” cells aren’t just sitting idly; they are actively contributing to the progression of these age-related diseases.
Understanding this connection is vital because it suggests new avenues for treatment. By targeting these senescent cells or their harmful secretions, scientists hope to develop therapies that could slow down or even prevent the progression of CKD and cardiac fibrosis, ultimately improving health outcomes as we age.
Source: link to paper