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细胞衰老与慢性创面的新认识

New insights into the role of cellular senescence and chronic wounds.

机构信息

Institute of Evolution and Biodiversity, College of Marine Life Sciences, Ocean University of China, Qingdao, China.

College of Marine Life Sciences, Ocean University of China, Qingdao, China.

出版信息

Front Endocrinol (Lausanne). 2024 Nov 4;15:1400462. doi: 10.3389/fendo.2024.1400462. eCollection 2024.

DOI:10.3389/fendo.2024.1400462
PMID:39558972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11570929/
Abstract

Chronic or non-healing wounds, such as diabetic foot ulcers (DFUs), venous leg ulcers (VLUs), pressure ulcers (PUs) and wounds in the elderly etc., impose significant biological, social, and financial burdens on patients and their families. Despite ongoing efforts, effective treatments for these wounds remain elusive, costing the United States over US$25 billion annually. The wound healing process is notably slower in the elderly, partly due to cellular senescence, which plays a complex role in wound repair. High glucose levels, reactive oxygen species, and persistent inflammation are key factors that induce cellular senescence, contributing to chronic wound failure. This suggests that cellular senescence may not only drive age-related phenotypes and pathology but also be a key mediator of the decreased capacity for trauma repair. This review analyzes four aspects: characteristics of cellular senescence; cytotoxic stressors and related signaling pathways; the relationship between cellular senescence and typical chronic non-healing wounds; and current and future treatment strategies. In theory, anti-aging therapy may influence the process of chronic wound healing. However, the underlying molecular mechanism is not well understood. This review summarizes the relationship between cellular senescence and chronic wound healing to contribute to a better understanding of the mechanisms of chronic wound healing.

摘要

慢性或非愈合性伤口,如糖尿病足溃疡(DFU)、静脉溃疡(VLU)、压疮(PU)和老年伤口等,给患者及其家庭带来了巨大的生物、社会和经济负担。尽管一直在努力,但这些伤口的有效治疗仍然难以实现,每年给美国造成超过 250 亿美元的损失。老年人的伤口愈合过程明显较慢,部分原因是细胞衰老,它在伤口修复中起着复杂的作用。高血糖水平、活性氧和持续的炎症是诱导细胞衰老的关键因素,导致慢性伤口失败。这表明细胞衰老不仅可能驱动与年龄相关的表型和病理学,而且可能是创伤修复能力下降的关键介质。本综述分析了四个方面:细胞衰老的特征;细胞毒性应激源及相关信号通路;细胞衰老与典型慢性非愈合性伤口的关系;以及当前和未来的治疗策略。理论上,抗衰老治疗可能会影响慢性伤口愈合的过程。然而,其潜在的分子机制尚不清楚。本综述总结了细胞衰老与慢性伤口愈合之间的关系,有助于更好地理解慢性伤口愈合的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2542/11570929/26f6ff3ab2cb/fendo-15-1400462-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2542/11570929/41084115af5b/fendo-15-1400462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2542/11570929/92707ccbf3be/fendo-15-1400462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2542/11570929/f351a868154d/fendo-15-1400462-g003.jpg
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