Meanwhile, our DNA isn’t perfect—mistakes happen, and exposure to things like pollution, stress, and unhealthy diets can damage it further, increasing the risk of diseases like cancer. While efficient DNA repair is essential for maintaining genome integrity, its efficacy diminishes with age. Epigenetic changes, including DNA methylation and histone modifications, regulate gene expression without altering the DNA sequence. These changes, influenced by factors such as diet and lifestyle, can disrupt normal cellular functions, contributing to aging through a process known as epigenetic drift.
Mitochondrial dysfunction results from mutations in mitochondrial DNA and increased production of reactive oxygen species (ROS), impairing cellular energy production and promoting oxidative damage. Senescence and apoptosis also play critical roles; senescent cells stop dividing but remain active, often secreting pro-inflammatory factors that disrupt tissue function, while apoptosis removes damaged cells but can lead to tissue degeneration if excessive. Proteostasis, or the balance of protein synthesis, folding, and degradation, declines with age, leading to an accumulation of misfolded proteins that impair cellular function and contribute to conditions like neurodegenerative diseases. Genetics and epigenetics further influence aging; genetic factors determine baseline longevity, with variations in genes related to DNA repair, antioxidant defenses, and metabolism significantly affecting the aging process. Key genes like SIRT1, FOXO, and mTOR are involved in stress resistance, metabolism, and lifespan regulation.
