Inflammatory cytokine signaling describes the complex, intercellular communication network mediated by small protein messengers, known as cytokines, that regulate the body’s inflammatory and immune responses. These signaling molecules, such as Interleukin-6 and Tumor Necrosis Factor-alpha, are released by immune cells and adipocytes, acting on distant target cells to orchestrate a systemic inflammatory cascade. Chronic dysregulation of this signaling pathway, often termed low-grade systemic inflammation, is a key driver of age-related diseases and metabolic dysfunction. Modulating this signaling is a major therapeutic target in promoting overall health and longevity.
Origin
The term combines Inflammatory, relating to the body’s protective reaction to injury or infection, with Cytokine, derived from the Greek cyto- for cell and kinos for movement, highlighting their role in cellular migration and communication. The concept of Signaling comes from molecular biology, describing the transmission of information across a cell membrane to induce a cellular response. This entire field gained significant clinical relevance with the recognition that chronic, low-level cytokine signaling links obesity and metabolic syndrome to cardiovascular disease.
Mechanism
The mechanism involves cytokines binding to specific receptors on target cells, activating intracellular signaling pathways, most notably the NF-κB pathway. Activation of NF-κB then translocates to the nucleus, promoting the transcription of genes that encode more inflammatory cytokines, creating a self-amplifying loop. In metabolic tissues, such as the liver and muscle, these signals interfere with insulin receptor substrate activity, leading directly to insulin resistance. This chronic, low-level inflammatory signaling essentially acts as a persistent metabolic brake, impairing glucose and lipid metabolism throughout the body.
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