Damage-Associated Molecular Patterns in Inflammatory Diseases
- PMID: 30181915
- PMCID: PMC6117512
- DOI: 10.4110/in.2018.18.e27
Damage-Associated Molecular Patterns in Inflammatory Diseases
Abstract
Damage-associated molecular patterns (DAMPs) are endogenous danger molecules that are released from damaged or dying cells and activate the innate immune system by interacting with pattern recognition receptors (PRRs). Although DAMPs contribute to the host's defense, they promote pathological inflammatory responses. Recent studies have suggested that various DAMPs, such as high-mobility group box 1 (HMGB1), S100 proteins, and heat shock proteins (HSPs), are increased and considered to have a pathogenic role in inflammatory diseases. Here, we review current research on the role of DAMPs in inflammatory diseases, including rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, atherosclerosis, Alzheimer's disease, Parkinson's disease, and cancer. We also discuss the possibility of DAMPs as biomarkers and therapeutic targets for these diseases.
Keywords: Damage-associated molecular patterns; Inflammation; Inflammatory diseases; Pattern recognition receptors.
Conflict of interest statement
Conflict of Interest: The authors declare no potential conflicts of interest.
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References
-
- Albiger B, Dahlberg S, Henriques-Normark B, Normark S. Role of the innate immune system in host defence against bacterial infections: focus on the Toll-like receptors. J Intern Med. 2007;261:511–528. - PubMed
-
- Lee MS, Kim YJ. Pattern-recognition receptor signaling initiated from extracellular, membrane, and cytoplasmic space. Mol Cells. 2007;23:1–10. - PubMed
-
- Feldman N, Rotter-Maskowitz A, Okun E. DAMPs as mediators of sterile inflammation in aging-related pathologies. Ageing Res Rev. 2015;24:29–39. - PubMed
-
- Medzhitov R. Inflammation 2010: new adventures of an old flame. Cell. 2010;140:771–776. - PubMed
-
- Scrivo R, Vasile M, Bartosiewicz I, Valesini G. Inflammation as “common soil” of the multifactorial diseases. Autoimmun Rev. 2011;10:369–374. - PubMed
