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Review
. 2013 Jul;64(7):481-8.
doi: 10.1007/s00105-012-2516-7.

[Current insights into the pathophysiology of rosacea]

[Article in German]
J Schauber  1 , B Homey, M Steinhoff
Affiliations
Review

[Current insights into the pathophysiology of rosacea]

[Article in German]
J Schauber et al. Hautarzt. 2013 Jul.

Abstract

Rosacea is a chronic inflammatory skin disease mainly affecting the face. Four major clinical subtypes of rosacea can be identified: erythemato-telangiectatic, papulopustular, phymatous and ocular rosacea. Still, it is currently unclear whether these subtypes develop consecutively or if any subtypes may occur individually as part of a syndrome. Rosacea is characterized by facial flushing, erythema, chronic inflammation, edema and fibrosis. Several trigger factors can worsen the disease or cause recurring episodes of inflammation. Although some aspects in the pathophysiology of rosacea have been characterized in more detail during the past years, the precise interplay of the various dysregulated systems is still poorly understood. In early disease manifestations and milder stages, dysfunction of neurovascular regulation and the innate immune system seem to be driving forces in rosacea pathophysiology. A disturbed chemokine and cytokine network further contributes to disease progression. This current review highlights some of the recent findings in rosacea pathophysiology and points out novel targets for therapeutic intervention.

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References

    1. J Invest Dermatol. 2009 Feb;129(2):460-7 - PubMed
    1. J Investig Dermatol Symp Proc. 2011 Dec;15(1):33-9 - PubMed
    1. Nature. 1997 Oct 23;389(6653):816-24 - PubMed
    1. J Biol Chem. 2011 Sep 30;286(39):34121-30 - PubMed
    1. J Dermatol Sci. 2009 Aug;55(2):77-81 - PubMed

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