Research Paper Volume 15, Issue 8 pp 2852—2862
A chronic wound model to investigate skin cellular senescence
- 1 Department of Dermatology, Mayo Clinic, Rochester, MN 55905, USA
- 2 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA
- 3 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA
- 4 Department of Medicine, Division of General Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA
Received: December 28, 2022 Accepted: April 3, 2023 Published: April 21, 2023
https://doi.org/10.18632/aging.204667How to Cite
Copyright: © 2023 Wyles et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Wound healing is an essential physiological process for restoring normal skin structure and function post-injury. The role of cellular senescence, an essentially irreversible cell cycle state in response to damaging stimuli, has emerged as a critical mechanism in wound remodeling. Transiently-induced senescence during tissue remodeling has been shown to be beneficial in the acute wound healing phase. In contrast, persistent senescence, as observed in chronic wounds, contributes to delayed closure. Herein we describe a chronic wound murine model and its cellular senescence profile, including the senescence-associated secretory phenotype.
Abbreviations
SASP: senescence-associated secretory phenotype; ECM: extracellular matrix; IACUC: Institutional Animal Care and Use Committee; ATZ: 3-amino-1,2,4-trizole; MSA: mercaptosuccinic acid; ISH: in situ hybridization; SMS: senescence messaging secretome.