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皮肤疾病炎症的发病机制:从分子机制到病理学。

Pathogenesis of Inflammation in Skin Disease: From Molecular Mechanisms to Pathology.

机构信息

Heersink School of Medicine, University of Alabama-Birmingham, Birmingham, AL 35233, USA.

College of Medicine, Florida State University, Tallahassee, FL 32306, USA.

出版信息

Int J Mol Sci. 2024 Sep 21;25(18):10152. doi: 10.3390/ijms251810152.


DOI:10.3390/ijms251810152
PMID:39337637
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11431851/
Abstract

Many skin diseases begin with inflammatory changes on a molecular level. To develop a more thorough understanding of skin pathology and to identify new targets for therapeutic advancements, molecular mechanisms of inflammation in the context of skin disease should be studied. Current research efforts to better understand skin disease have focused on examining the role of molecular processes at several stages of the inflammatory response such as the dysregulation of innate immunity sensors, disruption of both transcriptional and post-transcriptional regulation, and crosstalk between immune and neuronal processes (neuro-immune crosstalk). This review seeks to summarize recent developments in our understanding of inflammatory processes in skin disease and to highlight opportunities for therapeutic advancements. With a focus on publications within the past 5 years (2019-2024), the databases PubMed and EBSCOhost were used to search for peer-reviewed papers regarding inflammatory molecular mechanisms and skin disease. Several themes of research interest regarding inflammatory processes in skin disease were determined through extensive review and were included based on their relative representation in current research and their focus on therapeutic potential. Several skin diseases such as psoriasis, atopic dermatitis, hidradenitis suppurativa, and scleroderma were described in the paper to demonstrate the widespread influence of inflammation in skin disease.

摘要

许多皮肤疾病从分子层面的炎症变化开始。为了更深入地了解皮肤病理学,并确定治疗进展的新靶点,应该研究皮肤疾病背景下炎症的分子机制。目前,为了更好地理解皮肤疾病,研究工作的重点集中在研究炎症反应的几个阶段的分子过程,如先天免疫传感器的失调、转录和转录后调控的破坏,以及免疫和神经元过程之间的串扰(神经免疫串扰)。这篇综述旨在总结我们对皮肤疾病中炎症过程的理解的最新进展,并强调治疗进展的机会。本文重点关注过去 5 年(2019-2024 年)的出版物,使用 PubMed 和 EBSCOhost 数据库搜索有关炎症分子机制和皮肤疾病的同行评审论文。通过广泛的回顾,确定了皮肤疾病中炎症过程的几个研究重点,并根据它们在当前研究中的相对代表性及其对治疗潜力的关注程度将其纳入。本文描述了几种皮肤疾病,如银屑病、特应性皮炎、化脓性汗腺炎和硬皮病,以展示炎症在皮肤疾病中的广泛影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/ca5e9ffab0a0/ijms-25-10152-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/b79e3cec627d/ijms-25-10152-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/731be6fccc63/ijms-25-10152-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/8d65b3b90fde/ijms-25-10152-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/3e703ec58083/ijms-25-10152-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/2762ae08f4ab/ijms-25-10152-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/ca5e9ffab0a0/ijms-25-10152-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/b79e3cec627d/ijms-25-10152-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/731be6fccc63/ijms-25-10152-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/8d65b3b90fde/ijms-25-10152-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/3e703ec58083/ijms-25-10152-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/2762ae08f4ab/ijms-25-10152-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9868/11431851/ca5e9ffab0a0/ijms-25-10152-g006.jpg

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引用本文的文献

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Mapping Emerging Scientific Trends in Chronic Skin Disorders Using Machine Learning-Based Bibliometrics.

Bioengineering (Basel). 2025-8-20

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IRAK4 Targeting: A Breakthrough Approach to Combat Hidradenitis Suppurativa.

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[4]
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J Cosmet Dermatol. 2025-5

[5]
Comprehensive single-cell transcriptomic reveals different destinies of melanocytes and dynamic changes of immune microenvironment in a psychological stress-induced leukoderma and leukotrichia mouse model.

Mol Med. 2025-5-14

[6]
Dual Biologic Therapy for Psoriasis in a Patient with Atopic Dermatitis.

Psoriasis (Auckl). 2025-4-23

本文引用的文献

[1]
IRAK4 Is Overexpressed in Hidradenitis Suppurativa Skin and Correlates with Inflammatory Biomarkers.

J Invest Dermatol. 2025-2

[2]
Inflammasomes: emerging therapeutic targets in hidradenitis suppurativa?

Br J Dermatol. 2024-10-17

[3]
MicroRNA-939 amplifies induced matrix metalloproteinase expression in atopic dermatitis.

Front Immunol. 2024

[4]
Dysregulation of circulating collagen turnover markers in very early systemic sclerosis.

RMD Open. 2024-5-28

[5]
Deregulated Long Non-Coding RNAs (lncRNA) as Promising Biomarkers in Hidradenitis Suppurativa.

J Clin Med. 2024-5-20

[6]
Deciphering epigenetic regulations in the inflammatory pathways of atopic dermatitis.

Life Sci. 2024-7-1

[7]
Cutaneous inflammasome driving ASC / gasdermin-D activation and IL-1β-secreting macrophages in severe atopic dermatitis.

Arch Dermatol Res. 2024-5-11

[8]
Biosensing circulating MicroRNAs in autoinflammatory skin diseases: Focus on Hidradenitis suppurativa.

Front Genet. 2024-4-9

[9]
MicroRNA-21a-5p inhibition alleviates systemic sclerosis by targeting STAT3 signaling.

J Transl Med. 2024-4-1

[10]
The NLRP3 Inflammasome Gene Is Overexpressed in Hidradenitis Suppurativa Lesions: A Preliminary Study on the Role of Pyroptosis in Disease Pathogenesis.

Curr Issues Mol Biol. 2024-3-16

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