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Atrophic acne scar: A process from altered metabolism of elastic fibers and collagen fibers based on TGF-β1 signaling.

Br J Dermatol. 2019 Mar 01;:

Authors: Moon J, Yoon JY, Yang JH, Kwon HH, Min S, Suh DH

Abstract
BACKGROUND: Atrophic acne scar, a persistent sequela from acne, is undesirably troubling many patients in cosmetic and psychosocial aspects. Although there have been some reports to emphasize the role of early inflammatory responses in atrophic acne scarring, evolving perspectives on the detailed pathogenic process are promptly needed.
OBJECTIVES: Examining the histological, immunological and molecular changes in early acne lesions susceptible to atrophic scarring can provide new insights to understand the pathophysiology of atrophic acne scar.
METHODS: We experimentally validated several early fundamental hallmarks accounting for the transition of early acne lesions to atrophic scars by comparing molecular profiles of skin and acne lesions between patients who were prone to scar (APS) and not (ANS).
RESULTS: In APS, compared to ANS, devastating degradation of elastic fibers and collagen fibers occurred in the dermis, followed by their incomplete recovery. Abnormally excessive inflammation mediated by innate immunity with Th17/Th1 cells was observed. Epidermal proliferation was significantly diminished. TGF-β1 was drastically elevated in APS, suggesting that the aberrant TGF-β1 signaling is an underlying modulator of all these pathological processes.
CONCLUSIONS: These results may provide a basis for understanding the pathogenesis of atrophic acne scarring. Reduction of excessive inflammation and TGF-β1 signaling in early acne lesions is expected to facilitate the protection of normal extracellular matrix metabolism and the prevention of atrophic scar formation ultimately. This article is protected by copyright. All rights reserved.

PMID: 30822364 [PubMed - as supplied by publisher]

{url} = URL to article

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