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压力、适应性负荷和神经炎症:青光眼的种族和社会经济健康差异的影响。

Stress, Allostatic Load, and Neuroinflammation: Implications for Racial and Socioeconomic Health Disparities in Glaucoma.

机构信息

Department of Surgery, University of Utah, Salt Lake City, UT 84101, USA.

Scheie Eye Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Int J Mol Sci. 2024 Jan 29;25(3):1653. doi: 10.3390/ijms25031653.

DOI:10.3390/ijms25031653
PMID:38338933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10855412/
Abstract

Glaucoma is the leading cause of irreversible blindness, and its pathophysiology includes neuroinflammatory changes. The present therapies for glaucoma target pressure-lowering mechanisms with limited success, making neuroinflammation a target for future interventions. This review summarizes the neuroinflammatory pathways seen in glaucoma and their interplay with stress. Glucocorticoids have been shown to activate proinflammatory glial cells, contributing to the neuroinflammation in glaucoma. Glucocorticoids have also been shown to increase the IOP directly. Stress-associated autonomic dysfunction can affect the vascular homeostasis in the retina and create oxidative stress. Diabetes, hyperglycemic-mediated endothelial damage, and vascular inflammation also play important roles in the neuroinflammation in glaucoma and diabetic retinopathy. Psychosocial stress has been implicated in an increased IOP and glaucoma outcomes. People who experience maladaptive chronic stress suffer from a condition known as allostatic load, which describes pathologic neuroendocrine dysregulation. The effects of allostatic load and chronic stress have been studied in patients affected by a lower socioeconomic status (SES) and marginalized racial identities. A lower SES is associated with higher rates of glaucoma and also affects the access to care and screening. Additionally, people of African ancestry are disproportionately affected by glaucoma for reasons that are multifactorial. In conclusion, this review explores neuroinflammation in glaucoma, highlighting opportunities for future investigation.

摘要

青光眼是导致不可逆性失明的主要原因,其病理生理学包括神经炎症变化。目前治疗青光眼的方法主要针对降压机制,但效果有限,因此神经炎症成为未来干预的靶点。本综述总结了青光眼的神经炎症途径及其与应激的相互作用。研究表明,糖皮质激素可激活促炎神经胶质细胞,导致青光眼的神经炎症。糖皮质激素还被证明可以直接升高眼内压。与应激相关的自主神经功能障碍会影响视网膜的血管内稳态并产生氧化应激。糖尿病、高血糖介导的内皮损伤和血管炎症也在青光眼和糖尿病性视网膜病变的神经炎症中发挥重要作用。心理社会应激与眼压升高和青光眼结局有关。经历适应不良性慢性应激的人会出现一种称为“全身适应不良”的疾病,描述了病理性神经内分泌失调。已经在受较低社会经济地位(SES)和边缘化种族身份影响的患者中研究了全身适应不良和慢性应激的影响。较低的 SES 与更高的青光眼发病率相关,并且还会影响获得护理和筛查的机会。此外,非洲裔美国人不成比例地受到青光眼的影响,其原因是多因素的。总之,本综述探讨了青光眼的神经炎症,强调了未来研究的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5a9/10855412/22e2e02e19a3/ijms-25-01653-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5a9/10855412/22e2e02e19a3/ijms-25-01653-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5a9/10855412/22e2e02e19a3/ijms-25-01653-g001.jpg

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