This term refers to the progressive decline in the structural integrity and functional capacity of various tissues and organs that occurs as a natural consequence of biological aging. It encompasses cellular senescence, telomere attrition, and accumulation of molecular damage, leading to impaired tissue repair and reduced homeostatic reserve. The clinical manifestation of this dysfunction includes sarcopenia, decreased bone density, and reduced endocrine gland responsiveness.
Origin
The concept is foundational to gerontology and the biology of aging, drawing from the understanding that aging is characterized by a gradual loss of physiological efficiency. The term itself is descriptive, combining the temporal process of aging with the measurable impairment of tissue function, a central focus in longevity research and clinical anti-aging medicine. It is a unifying concept for diverse age-associated pathologies.
Mechanism
At the cellular level, dysfunction is driven by mitochondrial impairment, increased oxidative stress, and epigenetic alterations that disrupt gene expression necessary for optimal tissue maintenance. Hormonal changes, such as the age-related decline in growth hormone, sex steroids, and dehydroepiandrosterone (DHEA), further accelerate this process by reducing anabolic signaling and regenerative capacity. The accumulation of senescent cells, which secrete pro-inflammatory factors, also contributes significantly to the chronic low-grade inflammation, or inflammaging, characteristic of tissue decline.
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