The molecular pathology of rosacea

Abstract

Rosacea is a common and chronic inflammatory skin disease that affects over 10 million Americans. Although the phenotypes of rosacea are clinically heterogeneous, they are all related by the presence of chronic facial skin inflammation. Until recently, the pathophysiology of this disease has been poorly understood and limited to descriptions of factors that exacerbate or improve this disorder. Recent molecular studies suggest that an altered innate immune response is involved in the pathogenesis of the vascular and inflammatory disease seen in patients with rosacea. These findings may help explain the benefits of current treatments and suggest new therapeutic strategies helpful for alleviating this disease. This article discusses the possible molecular mechanisms for the pathogenesis of rosacea from current clinical observations and laboratory research.

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Figure. The possible molecular mechanisms for the pathogenesis of rosacea

Environmental changes, altered hormone balances and microbe challenges are sensed by TLRs (Toll-like receptors) and other pattern recognition receptors. TLRs signaling induce effecter molecules: cathelicidin, kallikrein, MMPs (matrix metalloproteinases), ROS (reactive oxygen species), NO (nitric oxides), cytokines, and chemokines. These effectors modify the dermal structure by vascular changes and collagen degeneration accompanied with inflammatory cells recruitments. Infiltrated neutrophils and lymphocytes will be the further source of effecter molecules, which activate TLRs directly and indirectly.