Molecular Aging refers to the cumulative, progressive accumulation of damage and dysfunction at the cellular and subcellular level that underlies the visible and functional decline of the human body over time. This includes quantifiable changes to DNA, proteins, lipids, and organelles, which collectively impair cellular homeostasis and regenerative capacity. Key hallmarks of this process include telomere shortening, epigenetic alterations, and mitochondrial decay, representing the fundamental biological basis of senescence. Understanding this molecular foundation is crucial for developing targeted longevity interventions.
Origin
The concept is foundational to the field of biogerontology, tracing its roots to the early theories of aging that proposed damage accumulation as the primary driver of senescence. It gained scientific precision with the discovery of specific molecular mechanisms, such as oxidative stress and DNA repair deficiencies, in the latter half of the 20th century. Modern research has consolidated these into the recognized “hallmarks of aging.”
Mechanism
The core mechanism involves an imbalance between damage accumulation and repair processes within the cell. Factors such as chronic low-grade inflammation and hormonal dysregulation accelerate this damage. For example, reduced growth hormone and DHEA signaling can impair protein synthesis and repair, while oxidative stress from metabolic byproducts damages mitochondrial DNA. These molecular lesions collectively disrupt cellular signaling pathways, leading to tissue and organ system failure.
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