Under conditions leading to aging and metabolic syndrome, the hypothalamus atypically undergoes proin-flammatory signaling activation leading to a chronic and stable background inflammation, referred to as "hypothalamic microinflammation." Through the past decade of research, progress has been made to causally link this hypothalamic inflammation to the mechanism of aging as well as metabolic syndrome, promoting the "hypothalamic microinflammation" theory, which helps characterize the consensus of these epidemic health problems. In general, it is consistently appreciated that hypothalamic microinflammation emerges during the early stages of aging and metabolic syndrome and evolves to be multifaceted and advanced alongside disease progression, while inhibition of key inflammatory components in the hypothalamus has a broad range of effects in counteracting these disorders. Herein, focusing on aging and metabolic syndrome, this writing aims to provide an overview of and insights into the mediators, signaling components, cellular impacts, and physiological significance of this hypothalamic microinflammation.
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