Intercellular communication networks represent the complex system of signaling pathways and molecules that govern the interaction and coordination between individual cells within a tissue and across different organ systems. These networks utilize diverse chemical messengers, including hormones, neurotransmitters, cytokines, and growth factors, to regulate essential physiological processes like growth, metabolism, and immune response. Disruption of these networks, often through chronic inflammation or the accumulation of Senescence-Associated Secretory Phenotype (SASP) factors, is a central driver of age-related dysfunction. Maintaining the fidelity of these signaling channels is essential for systemic health and tissue integrity.
Origin
The term is a conceptual construct from cell biology and systems biology, integrating the basic biological process of “intercellular communication” with the structural concept of “networks” to emphasize complexity and interconnectedness. Its foundation lies in the discovery of paracrine and endocrine signaling, recognizing that cells do not operate in isolation. In the context of aging, the term has gained prominence to describe the progressive “noise” or dysregulation in signaling pathways that accompanies biological decline.
Mechanism
The mechanism of communication relies on a precise system of ligand-receptor binding, where a signaling molecule released by one cell binds to a specific receptor on a target cell, initiating an intracellular cascade. Hormonal communication, a key part of this network, involves endocrine cells releasing hormones into the bloodstream to act on distant target tissues, regulating metabolism and reproduction. The network’s function is compromised by aging, often due to decreased receptor sensitivity, altered post-receptor signaling, or the pathological secretion of inhibitory or inflammatory molecules from senescent cells, thereby corrupting the systemic signaling environment.
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