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Damage-associated molecular pattern molecules (DAMPs) are endogenous molecules released by stressed, damaged, or dying cells. They act as danger signals to the immune system, alerting it to tissue injury or cellular stress in the absence of infection. DAMPs are recognized by pattern recognition receptors (PRRs) on immune cells, initiating a non-infectious inflammatory response that helps clear damaged tissue and promote healing. While DAMP signaling is essential for normal wound healing and defense against injury, excessive or chronic release of DAMPs can drive pathological inflammation seen in various diseases. Targeting specific DAMP molecules or their interactions with PRRs represents an emerging therapeutic strategy.
DAMPs bind to pattern recognition receptors (PRRs) such as TLRs, NLRs, and CLRs, initiating intracellular signaling cascades that lead to the production of inflammatory cytokines and chemokines. Therapeutic strategies aim to block the interaction of DAMPs with PRRs or inhibit downstream signaling pathways.
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