Abstract
The concept of damage-associated molecular patterns (DAMPs), derived
from Polly Matzinger’s danger hypothesis in 1994, provides a theoretical
framework for understanding immune system recognition and response to
cellular distress in the absence of pathogens. DAMPs, released by
stressed, dying, or dead cells, serve as host signals that initiate,
sustain, and amplify inflammatory responses. These molecular patterns
are essential in mediating the interaction between innate and adaptive
immunity, elucidating the mechanisms behind immune cell recruitment and
activation across a range of pathological states. This review
systematically explores the evolution of the DAMP hypothesis, detailing
the classification, biogenesis, and cellular origins of DAMPs, along
with their associated signaling pathways and release mechanisms.
Furthermore, it discusses the clinical implications of DAMPs and
examines their therapeutic potential in various pathological conditions,
underscoring their increasing significance in medical research and
therapeutic innovation.