Mitochondrial dysfunction is a key player, leading to a decline in energy production and an increase in damaging reactive oxygen species (ROS). This, in turn, exacerbates cellular senescence, where cells enter a state of irreversible growth arrest and secrete inflammatory factors that can harm surrounding tissues.

Communication between cells also falters with age, often due to dysregulation of signaling pathways like NF-kB, which is crucial for immune responses and inflammation. Genomic instability, marked by an accumulation of DNA damage, and telomere attrition, the progressive shortening of the protective ends of chromosomes, both contribute significantly to cellular aging.
Nutrient sensing pathways, including those regulated by AMPK and mTOR, become deregulated, disrupting the balance of cellular metabolism and growth. The exhaustion of stem cells impairs the body's regenerative potential, while the loss of proteostasis leads to an accumulation of dysfunctional proteins.

Lastly, epigenetic alterations, which involve changes to DNA and histone modifications, can shift gene expression patterns and affect cellular function. Proteins such as sirtuins (SIRTs) play a pivotal role in managing these epigenetic changes and are vital to maintaining cellular health and longevity.