Tissue engineering strategies to bioengineer the ageing skin phenotype in vitro

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Human skin ageing is a complex and heterogeneous process, which is influenced by genetically determined intrinsic factors and accelerated by cumulative exposure to extrinsic stressors. In the current world ageing demographic, there is a requirement for a bioengineered ageing skin model, to further the understanding of the intricate molecular mechanisms of skin ageing, and provide a distinct and biologically relevant platform for testing actives and formulations. There have been many recent advances in the development of skin models that recapitulate aspects of the ageing phenotype in vitro. This review encompasses the features of skin ageing, the molecular mechanisms that drive the ageing phenotype, and tissue engineering strategies that have been utilised to bioengineer ageing skin in vitro.

Abstract

In the world ageing population, there is a demand for bioengineered ageing skin models, to further understanding of the molecular mechanisms of skin ageing and provide a predictive in vitro platform for testing of anti‐ageing actives. This review explores the features of ageing skin, molecular mechanisms that drive the ageing skin phenotype, and discusses how tissue engineering strategies can be applied to model this phenomenon in vitro.

Related collections

Most cited references 129

Record: found
Abstract: found
Article: found

The Hallmarks of Aging

Carlos López-Otín, Maria Blasco, Linda Partridge … (2014)

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.

0 comments Cited 3466 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

ROS function in redox signaling and oxidative stress.

Michael Schieber, Navdeep S. Chandel (2014)

Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins and DNA. Oxidative stress has been linked to a myriad of pathologies. However, elevated ROS also act as signaling molecules in the maintenance of physiological functions--a process termed redox biology. In this review we discuss the two faces of ROS--redox biology and oxidative stress--and their contribution to both physiological and pathological conditions. Redox biology involves a small increase in ROS levels that activates signaling pathways to initiate biological processes, while oxidative stress denotes high levels of ROS that result in damage to DNA, protein or lipids. Thus, the response to ROS displays hormesis, given that the opposite effect is observed at low levels compared with that seen at high levels. Here, we argue that redox biology, rather than oxidative stress, underlies physiological and pathological conditions. Copyright © 2014 Elsevier Ltd. All rights reserved.

0 comments Cited 1215 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

How mitochondria produce reactive oxygen species

Michael P. Murphy (2008)

The production of ROS (reactive oxygen species) by mammalian mitochondria is important because it underlies oxidative damage in many pathologies and contributes to retrograde redox signalling from the organelle to the cytosol and nucleus. Superoxide (O2 •−) is the proximal mitochondrial ROS, and in the present review I outline the principles that govern O2 •− production within the matrix of mammalian mitochondria. The flux of O2 •− is related to the concentration of potential electron donors, the local concentration of O2 and the second-order rate constants for the reactions between them. Two modes of operation by isolated mitochondria result in significant O2 •− production, predominantly from complex I: (i) when the mitochondria are not making ATP and consequently have a high Δp (protonmotive force) and a reduced CoQ (coenzyme Q) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For mitochondria that are actively making ATP, and consequently have a lower Δp and NADH/NAD+ ratio, the extent of O2 •− production is far lower. The generation of O2 •− within the mitochondrial matrix depends critically on Δp, the NADH/NAD+ and CoQH2/CoQ ratios and the local O2 concentration, which are all highly variable and difficult to measure in vivo. Consequently, it is not possible to estimate O2 •− generation by mitochondria in vivo from O2 •−-production rates by isolated mitochondria, and such extrapolations in the literature are misleading. Even so, the description outlined here facilitates the understanding of factors that favour mitochondrial ROS production. There is a clear need to develop better methods to measure mitochondrial O2 •− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

0 comments Cited 1182 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Stefan Przyborski: stefan.przyborski@durham.ac.uk

Journal

Journal ID (nlm-ta): Aging Cell

Journal ID (iso-abbrev): Aging Cell

Journal ID (doi): 10.1111/(ISSN)1474-9726

Journal ID (publisher-id): ACEL

Title: Aging Cell

Publisher: John Wiley and Sons Inc. (Hoboken )

ISSN (Print): 1474-9718

ISSN (Electronic): 1474-9726

Publication date (Electronic): 17 January 2022

Publication date (Print): February 2022

Volume: 21

Issue: 2 ( doiID: 10.1111/acel.v21.2 )

Electronic Location Identifier: e13550

Affiliations

[ ¹ ] Department of Biosciences Durham University Durham UK

[ ² ] Procter and Gamble Mason Business Center Cincinnati Ohio USA

[ ³ ] Institute for Cell and Molecular Sciences Newcastle University Newcastle Upon Tyne UK

[ ⁴ ] Reprocell Europe Glasgow, Durham UK

Author notes

[*] [* ] Correspondence

Stefan Przyborski, Department of Biosciences, Durham University, Durham, UK.

Email: stefan.przyborski@ 123456durham.ac.uk

Author information

Lydia Costello https://orcid.org/0000-0002-9370-0019

Article

Publisher ID: ACEL13550

DOI: 10.1111/acel.13550

PMC ID: 8844123

PubMed ID: 35037366

SO-VID: 9d3a90d2-03d3-4093-bdf9-12e2691af8ca

License:

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

History

Date revision received : 14 December 2021

Date received : 05 November 2021

Date accepted : 29 December 2021

Page count

Figures: 5, Tables: 1, Pages: 19, Words: 13578

Funding

Funded by: Biotechnology and Biological Sciences Research Council , doi 10.13039/501100000268;

Award ID: BB/K019260/1

Award ID: BB/M011186/1

Custom metadata

source-schema-version-number 2.0

cover-date February 2022

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.1.1 mode:remove_FC converted:14.02.2022

ScienceOpen disciplines: Cell biology

Keywords: ageing,bioengineered tissue,human,in vitro,molecular biology of aging,skin

Data availability:

ScienceOpen disciplines: Cell biology

Keywords: ageing, bioengineered tissue, human, in vitro, molecular biology of aging, skin

Tissue engineering strategies to bioengineer the ageing skin phenotype in vitro

Read this article at

Abstract

Abstract

Related collections

Inflamed lung in vitro co-culture models

Most cited references 129

The Hallmarks of Aging

ROS function in redox signaling and oxidative stress.

How mitochondria produce reactive oxygen species

Author and article information

Contributors

Journal

Affiliations

Author notes

Author information

Article

History

Page count

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 120

Cited by 3

Most referenced authors 3,125