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Skin ageing: Skin ageing

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TLDR
The formation of reactive oxygen species and the induction of matrix metalloproteinases reflect the central aspects of skin ageing and the detection of its mechanisms have furthered the development of various therapeutic and preventive strategies.
Abstract
Similar to the entire organism, skin is subject to an unpreventable intrinsic ageing process. Additionally, skin ageing is also influenced by exogenous factors. Ultraviolet radiation in particular results in premature skin ageing, also referred to as extrinsic skin ageing or photoageing, which is the main cause of the changes associated with the ageing process in sun‐exposed areas. Despite their morphological and pathophysiological differences, intrinsic and extrinsic ageing share several molecular similarities. The formation of reactive oxygen species and the induction of matrix metalloproteinases reflect the central aspects of skin ageing. Accumulation of fragmented collagen fibrils prevents neocollagenesis and accounts for the further degradation of the extracellular matrix by means of positive feedback regulation. The importance of extrinsic factors in skin ageing and the detection of its mechanisms have furthered the development of various therapeutic and preventive strategies.

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The extracellular matrix at a glance

TL;DR: The extracellular matrix is the non-cellular component present within all tissues and organs, and provides not only essential physical scaffolding for the cellular constituents but also initiates crucial biochemical and biomechanical cues that are required for tissue development.
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Oxidative Stress in Aging Human Skin

TL;DR: In this review the overall effects of oxidative stress are discussed as well as the sources of ROS including the mitochondrial ETC, peroxisomal and ER localized proteins, the Fenton reaction, and such enzymes as cyclooxygenase, lipoxygenases, xanthine oxidases, and NADPH oxidases.
Journal ArticleDOI

Fighting against Skin Aging: The Way from Bench to Bedside.

TL;DR: This review summarizes changes in skin aging, research advances of the molecular mechanisms leading to these changes, and the treatment strategies aimed at preventing or reversing skin aging.
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Introduction to skin aging

TL;DR: The topic of human skin aging is introduced, with a focus on how maintenance of function in this complex multi-cell type organ is key for retaining quality of life into old age.
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Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair

TL;DR: Variation in healing and scarring rates in multiple tissues suggests that fibroblast diversity exists, and functionally distinct subsets of myofibroblast subsets in skin wound beds from adult mice are defined.
References
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Journal ArticleDOI

The limited in vitro lifetime of human diploid cell strains

TL;DR: The survival curves obtained with human diploid cell strains are comparable to “multiple-hit” or “ multiple-target” curves obtain with other biological systems where an initial threshold dose is required before an exponential form of the curve is established.
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Telomeres shorten during ageing of human fibroblasts.

TL;DR: The amount and length of telomeric DNA in human fibroblasts does in fact decrease as a function of serial passage during ageing in vitro and possibly in vivo.
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Oxidative Stress, Caloric Restriction, and Aging

TL;DR: Support for this hypothesis includes the following observations: (i) Overexpression of antioxidative enzymes retards the age-related accrual of oxidative damage and extends the maximum life-span of transgenic Drosophila melanogaster and (ii) Variations in longevity among different species inversely correlate with the rates of mitochondrial generation of the superoxide anion radical and hydrogen peroxide.
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Mechanisms of photoaging and chronological skin aging

TL;DR: This article reviews the current understanding and presents new data about the molecular pathways that mediate skin damage by UV irradiation and by the passage of time and reveals that chronological aging and photoaging share fundamental molecular pathways.
Journal ArticleDOI

Molecular basis of sun-induced premature skin ageing and retinoid antagonism

TL;DR: It is proposed that elevated metalloprotein-ases, resulting from activation of AP-1 and NF-KB by low-dose solar irradiation, degrade collagen and elastin in skin, which would result in solar scars, which through accumulation from a lifetime of repeated low- dose sunlight exposure could cause premature skin ageing (photoageing).
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