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内源性特异性促消退介质在肥大细胞中的作用及其在炎症和消退过程中的参与情况。

The Role of Endogenous Specialized Proresolving Mediators in Mast Cells and Their Involvement in Inflammation and Resolution.

作者信息

Fukuishi Nobuyuki, Takahama Kentaro, Kurosaki Hiromasa, Ono Sayaka, Asai Haruka

机构信息

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kinjo Gakuin University, Nagoya 463-8521, Japan.

Technology Center, Tokai National Higher Education and Research System, Nagoya 464-8601, Japan.

出版信息

Int J Mol Sci. 2025 Feb 11;26(4):1491. doi: 10.3390/ijms26041491.

Abstract

Many polyunsaturated fatty acids within cells exhibit diverse physiological functions. Particularly, arachidonic acid is the precursor of highly bioactive prostaglandins and leukotrienes, which are pro-inflammatory mediators. However, polyunsaturated fatty acids, such as arachidonic, docosahexaenoic, and eicosapentaenoic acids, can be metabolized into specialized proresolving mediators (SPMs), which have anti-inflammatory properties. Given that pro-inflammatory mediators and SPMs are produced via similar enzymatic pathways, SPMs can play a crucial role in mitigating excessive tissue damage induced by inflammation. Mast cells are immune cells that are widely distributed and strategically positioned at interfaces with the external environment, such as the skin and mucosa. As immune system sentinels, they respond to harmful pathogens and foreign substances. Upon activation, mast cells release various pro-inflammatory mediators, initiating an inflammatory response. Furthermore, these cells secrete factors that promote tissue repair and inhibit inflammation. This dual function positions mast cells as central regulators, balancing between the body's defense mechanisms and the need to minimize tissue injury. This review investigates the production of SPMs by mast cells and their subsequent effects on these cells. By elucidating the intricate relationship between mast cells and SPMs, this review aims to provide a comprehensive understanding of the mechanism by which these cells regulate the delicate balance between tissue damage and repair at inflammatory sites, ultimately contributing to the resolution of inflammatory responses.

摘要

细胞内的许多多不饱和脂肪酸具有多种生理功能。特别是,花生四烯酸是高生物活性前列腺素和白三烯的前体,而这些都是促炎介质。然而,多不饱和脂肪酸,如花生四烯酸、二十二碳六烯酸和二十碳五烯酸,可以代谢为具有抗炎特性的特殊促消退介质(SPM)。鉴于促炎介质和SPM是通过相似的酶促途径产生的,SPM在减轻炎症引起的过度组织损伤中可发挥关键作用。肥大细胞是广泛分布且战略性地定位在与外部环境的界面处(如皮肤和黏膜)的免疫细胞。作为免疫系统的哨兵,它们对有害病原体和外来物质作出反应。激活后,肥大细胞释放各种促炎介质,引发炎症反应。此外,这些细胞分泌促进组织修复和抑制炎症的因子。这种双重功能使肥大细胞成为核心调节因子,在机体防御机制和尽量减少组织损伤的需求之间取得平衡。本综述研究了肥大细胞产生SPM的情况及其对这些细胞的后续影响。通过阐明肥大细胞与SPM之间的复杂关系,本综述旨在全面了解这些细胞在炎症部位调节组织损伤与修复之间微妙平衡的机制,最终促进炎症反应的消退。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c16/11855587/d15d58690cef/ijms-26-01491-g001.jpg

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