Damage to skin extracellular matrix induced by UV exposureCitation formats

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Damage to skin extracellular matrix induced by UV exposure. / Watson, Rachel E B; Gibbs, Neil K.; Griffiths, Christopher E M; Sherratt, Michael J.

In: Antioxidants and Redox Signaling, Vol. 21, No. 7, 01.09.2014, p. 1063-1077.

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Watson, Rachel E B ; Gibbs, Neil K. ; Griffiths, Christopher E M ; Sherratt, Michael J. / Damage to skin extracellular matrix induced by UV exposure. In: Antioxidants and Redox Signaling. 2014 ; Vol. 21, No. 7. pp. 1063-1077.

Bibtex

@article{7c2ebcdb33c142ceb43cddbf00180d60,
title = "Damage to skin extracellular matrix induced by UV exposure",
abstract = "Significance: Chronic exposure to environmental ultraviolet radiation (UVR) plays a key role in both photocarcinogenesis and induction of accelerated skin aging. Although the spatiotemporal consequences of UVR exposure for the composition and architecture of the dermal extracellular matrix (ECM) are well characterized, the pathogenesis of photoaging remains poorly defined. Given the compelling evidence for the role of reactive oxygen species (ROS) as mediators of photoaging, UVR-exposed human skin may be an accessible model system in which to characterize the role of oxidative damage in both internal and external tissues. Recent Advances: Although the cell-mediated degradation of dermal components via UVR-induced expression of ECM proteases has long been identified as an integral part of the photoaging pathway, the relative importance and identity of cellular and extracellular photosensitizers (direct hit and bystanders models, respectively) in initiating this enzymatic activity is unclear. Recently, both age-related protein glycation and relative amino-acid composition have been identified as potential risk factors for photo-ionization and/or photo-sensitization. Here, we propose a selective multi-hit model of photoaging. Critical Issues: Bioinformatic analyses can be employed to identify candidate UVR targets/photosensitizers, but the action of UVR on protein structure and/or ROS production should be verified experimentally. Crucially, in the case of biochemically active ECM components such as fibronectin and fibrillin, the downstream effects of photo-degradation on tissue homeostasis remain to be confirmed. Future Directions: Both topical antioxidants and inhibitors of detrimental cell signaling may be effective in abrogating the effects of specific UVR-mediated protein degradation in the dermis. {\textcopyright} Copyright 2014, Mary Ann Liebert, Inc. 2014.",
author = "Watson, {Rachel E B} and Gibbs, {Neil K.} and Griffiths, {Christopher E M} and Sherratt, {Michael J.}",
note = "Times Cited: 0 0",
year = "2014",
month = sep,
day = "1",
doi = "10.1089/ars.2013.5653",
language = "English",
volume = "21",
pages = "1063--1077",
journal = "Antioxidants & redox signaling",
issn = "1523-0864",
publisher = "Mary Ann Liebert Incorporated",
number = "7",

}

RIS

TY - JOUR

T1 - Damage to skin extracellular matrix induced by UV exposure

AU - Watson, Rachel E B

AU - Gibbs, Neil K.

AU - Griffiths, Christopher E M

AU - Sherratt, Michael J.

N1 - Times Cited: 0 0

PY - 2014/9/1

Y1 - 2014/9/1

N2 - Significance: Chronic exposure to environmental ultraviolet radiation (UVR) plays a key role in both photocarcinogenesis and induction of accelerated skin aging. Although the spatiotemporal consequences of UVR exposure for the composition and architecture of the dermal extracellular matrix (ECM) are well characterized, the pathogenesis of photoaging remains poorly defined. Given the compelling evidence for the role of reactive oxygen species (ROS) as mediators of photoaging, UVR-exposed human skin may be an accessible model system in which to characterize the role of oxidative damage in both internal and external tissues. Recent Advances: Although the cell-mediated degradation of dermal components via UVR-induced expression of ECM proteases has long been identified as an integral part of the photoaging pathway, the relative importance and identity of cellular and extracellular photosensitizers (direct hit and bystanders models, respectively) in initiating this enzymatic activity is unclear. Recently, both age-related protein glycation and relative amino-acid composition have been identified as potential risk factors for photo-ionization and/or photo-sensitization. Here, we propose a selective multi-hit model of photoaging. Critical Issues: Bioinformatic analyses can be employed to identify candidate UVR targets/photosensitizers, but the action of UVR on protein structure and/or ROS production should be verified experimentally. Crucially, in the case of biochemically active ECM components such as fibronectin and fibrillin, the downstream effects of photo-degradation on tissue homeostasis remain to be confirmed. Future Directions: Both topical antioxidants and inhibitors of detrimental cell signaling may be effective in abrogating the effects of specific UVR-mediated protein degradation in the dermis. © Copyright 2014, Mary Ann Liebert, Inc. 2014.

AB - Significance: Chronic exposure to environmental ultraviolet radiation (UVR) plays a key role in both photocarcinogenesis and induction of accelerated skin aging. Although the spatiotemporal consequences of UVR exposure for the composition and architecture of the dermal extracellular matrix (ECM) are well characterized, the pathogenesis of photoaging remains poorly defined. Given the compelling evidence for the role of reactive oxygen species (ROS) as mediators of photoaging, UVR-exposed human skin may be an accessible model system in which to characterize the role of oxidative damage in both internal and external tissues. Recent Advances: Although the cell-mediated degradation of dermal components via UVR-induced expression of ECM proteases has long been identified as an integral part of the photoaging pathway, the relative importance and identity of cellular and extracellular photosensitizers (direct hit and bystanders models, respectively) in initiating this enzymatic activity is unclear. Recently, both age-related protein glycation and relative amino-acid composition have been identified as potential risk factors for photo-ionization and/or photo-sensitization. Here, we propose a selective multi-hit model of photoaging. Critical Issues: Bioinformatic analyses can be employed to identify candidate UVR targets/photosensitizers, but the action of UVR on protein structure and/or ROS production should be verified experimentally. Crucially, in the case of biochemically active ECM components such as fibronectin and fibrillin, the downstream effects of photo-degradation on tissue homeostasis remain to be confirmed. Future Directions: Both topical antioxidants and inhibitors of detrimental cell signaling may be effective in abrogating the effects of specific UVR-mediated protein degradation in the dermis. © Copyright 2014, Mary Ann Liebert, Inc. 2014.

U2 - 10.1089/ars.2013.5653

DO - 10.1089/ars.2013.5653

M3 - Article

C2 - 24124905

VL - 21

SP - 1063

EP - 1077

JO - Antioxidants & redox signaling

JF - Antioxidants & redox signaling

SN - 1523-0864

IS - 7

ER -