The progressive deterioration of signaling pathways and molecular interactions between cells, tissues, and organs that characterizes the aging process. This decline includes reduced receptor sensitivity, altered cytokine and chemokine profiles, and impaired paracrine and endocrine signaling efficiency. A breakdown in this complex, interconnected network of communication leads to dysregulation in homeostasis, chronic low-grade inflammation (inflammaging), and impaired tissue repair. Restoring clear cellular dialogue is a central focus of longevity research.
Origin
This concept stems from the molecular biology of aging, specifically the recognized “Hallmarks of Aging,” where altered intercellular communication is identified as a primary driver of senescence. The term synthesizes the physiological reality of aging with the fundamental biological process of cell-to-cell signaling. Understanding its origins requires examining the cumulative effects of oxidative stress, telomere attrition, and genetic instability on signaling molecules and receptor integrity.
Mechanism
The mechanism involves multiple molecular pathways, most notably the decline in sensitivity to key endocrine signals, such as insulin and growth factors, and the accumulation of senescent cells that secrete a pro-inflammatory senescence-associated secretory phenotype (SASP). This SASP disrupts local tissue environments and propagates systemic inflammation, further degrading communication. Interventions often target clearing senescent cells or employing peptides and small molecules to enhance receptor function and restore youthful signaling patterns, improving the clarity of systemic biological messages.
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