Stem cells lose their ability to divide as we age, and we are unable to replace cells that have migrated, differentiated, or died. As a result, we show outward symptoms of aging, such as gray hair.
As cells age, their mitochondria start to lose their integrity due to the build-up of oxidative stress. Compromised mitochondrial function leads to a number of adverse events, such as increased apoptosis induction, that correlate with aging.
Shortened telomeres are associated with aging cells that are senescent. As cells divide, the telomere ends of chromosomes get shorter. Eventually, telomerase gets silenced and the telomeres are too short for cells to divide.
As cells are exposed to environmental factors, they are subject to changes in their genome through epigenetic mechanisms. Such changes accumulate over time and have been correlated with the decline observed in aging cells.
As cells age, they show an increase in self-preserving signals that result in damage elsewhere. Altered extracellular communication with aging contributes to decline in tissue health.
As cells age, environmental stresses add up and mechanisms responsible for maintaining proper protein composition start to decline. Proteins lose their stability, autophagic processes start to fail, and misfolded proteins accumulate.