Role of Atypical Chemokines and Chemokine Receptors Pathways In the Pathogenesis of COPD
- Publisher:
- Bentham Science Publishers Ltd.
- Publication Type:
- Journal Article
- Citation:
- Current medicinal chemistry, 2020, 27
- Issue Date:
- 2020-08-19
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| Filename | Description | Size | |||
|---|---|---|---|---|---|
| Role of Atypical chemokines and chemokine receptors pathways in the pathogenesis of COPD.pdf | Published version | 2.98 MB |
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Chronic obstructive pulmonary disease (COPD) represents a heightened inflammatory
response in the lung generally resulting from tobacco smoking-induced recruitment and
activation of inflammatory cells and/or activation of lower airway structural cells. Several
mediators can modulate activation and recruitment of these cells, particularly those belonging
to the chemokines (conventional and atypical) family. There is emerging evidence for complex
roles of atypical chemokines and their receptors [such as high mobility group box 1
(HMGB1), antimicrobial peptides, receptor for advanced glycosylation end products (RAGE)
or toll-like receptors (TLRs)] in the pathogenesis of COPD, both in the stable disease and during
exacerbations. Modulators of these pathways represent potential novel therapies for
COPD and many are now in preclinical development. Inhibition of only a single atypical
chemokine or receptor may not block inflammatory processes because there is redundancy in
this network. However, there are many animal studies that encourage studies for modulating
the atypical chemokine network in COPD. Thus, few pharmaceutical companies maintain a
significant interest in developing agents that target these molecules as potential antiinflammatory
drugs. Antibody-based (biological) and small molecule drug (SMD)-based
therapies targeting atypical chemokines and/or their receptors are mostly at the preclinical
stage and their progression to clinical trials is eagerly awaited. These agents will most likely
enhance our knowledge about the role of atypical chemokines in COPD pathophysiology and
thereby improve COPD management.
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