Abstract

Sepsis refers to the deleterious and non-resolving systemic inflammatory response of the host to microbial infection and is the leading cause of death in intensive care units. The pathogenesis of sepsis is highly complex. It is principally attributable to dysregulation of the innate immune system. Damage-associated molecular patterns (DAMPs) are actively secreted by innate immune cells and/or released passively by injured or damaged cells in response to infection or injury. In the present review, we highlight emerging evidence that supports the notion that extracellular DAMPs act as crucial proinflammatory danger signals. Furthermore, we discuss the potential of a wide array of DAMPs as therapeutic targets in sepsis.

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