A Chronic Wound Model to Investigate Skin Cellular Senescence | Aging-US
Channel: Aging (Aging-US)
Date: 2023-04-30

Aging-US published this research paper as the cover for Volume 15, Issue 8, entitled, "A chronic wound model to investigate skin cellular senescence" by researchers from the Department of Dermatology, Mayo Clinic, Rochester, MN; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; Department of Medicine, Division of General Internal Medicine, Mayo Clinic, Rochester, MN.
@MayoClinic 
#aging  #research  #skin  #researchpaper  #openscience  #peerreview  #journal  #publication  #meded  #woundhealing  #senescence #cells 

DOI - https://doi.org/10.18632/aging.204667

Corresponding authors - James L. Kirkland - kirkland.james@mayo.edu, and Tamar Tchkonia - tchkonia.tamar@mayo.edu

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.

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Keywords - aging, wound healing, cellular senescence, chronic wound, re-epithelization, skin

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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