Unraveling complex mechanisms of telomere biology is central to understanding the close link between aging and inflammation. Telomeres are repetitive heterochromatin DNA structures at the ends of eukaryotic chromosomes, and their length is universally accepted as a marker of biological aging. Telomeres progressively shorten with every cell division until they ultimately trigger cellular senescence and apoptosis. Telomere shortening is also promoted by chronic inflammation and oxidative stress. Chronic inflammation and oxidative stress have been shown to be key drivers of age-related diseases, including neurodegeneration, cardiovascular disease, and cancer. Telomerase is central regulator at the intersection of genomic stability, mitochondrial function, epigenetic integrity, and proteostasis. Through its direct and indirect actions, telomerase modulates inflammatory pathways that drive aging and age-related diseases, highlighting its potential as a therapeutic target to mitigate inflammaging and extend healthspan.
Baylie et al. (2026) studied this question.