Literature DB >> 21175578

Does airway smooth muscle express an inflammatory phenotype in asthma?

Gautam Damera1, Reynold A Panettieri.   

Abstract

In addition to hyperresponsiveness in asthma, airway smooth muscle (ASM) also manifests an inflammatory phenotype characterized by augmented expression of mediators that enhance inflammation, contribute to tissue remodelling and augment leucocyte trafficking and activity. Our present review summarizes contemporary understanding of ASM-derived mediators and their paracrine and autocrine actions in airway diseases.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.

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Year:  2011        PMID： 21175578      PMCID： PMC3085869          DOI： 10.1111/j.1476-5381.2010.01165.x

Source DB:  PubMed          Journal:  Br J Pharmacol        ISSN： 0007-1188            Impact factor:   8.739


  159 in total

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4.  Interleukin-9 influences chemokine release in airway smooth muscle: role of ERK.

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5.  IFN-gamma inhibits human airway smooth muscle cell proliferation by modulating the E2F-1/Rb pathway.

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6.  Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice.

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Review 8.  Cellular regulation of RGS proteins: modulators and integrators of G protein signaling.

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  23 in total

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2.  Special issue of BJP on respiratory pharmacology.

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Review 3.  Asthma therapy and its effect on airway remodelling.

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Review 5.  A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.

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Review 6.  CD38 and airway hyper-responsiveness: studies on human airway smooth muscle cells and mouse models.

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Review 7.  CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.

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9.  TLR3 activation increases chemokine expression in human fetal airway smooth muscle cells.

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Review 10.  Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.

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