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脂质介导的病理学中的补体系统。

The complement system in lipid-mediated pathologies.

作者信息

Alic Lejla, Dendinovic Kristina, Papac-Milicevic Nikolina

机构信息

Department of Medical Biochemistry, Faculty of Medicine, University of Sarajevo, Sarajevo, Bosnia and Herzegovina.

Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.

出版信息

Front Immunol. 2024 Nov 20;15:1511886. doi: 10.3389/fimmu.2024.1511886. eCollection 2024.

DOI:10.3389/fimmu.2024.1511886
PMID:39635529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11614835/
Abstract

The complement system, a coordinator and facilitator of the innate immune response, plays an essential role in maintaining host homeostasis. It promotes clearance of pathogen- and danger-associated molecular patterns, regulates adaptive immunity, and can modify various metabolic processes such as energy expenditure, lipid metabolism, and glucose homeostasis. In this review, we will focus on the intricate interplay between complement components and lipid metabolism. More precisely, we will display how alterations in the activation and regulation of the complement system affect pathological outcome in lipid-associated diseases, such as atherosclerosis, obesity, metabolic syndrome, age-related macular degeneration, and metabolic dysfunction-associated steatotic liver disease. In addition to that, we will present and evaluate underlying complement-mediated physiological mechanisms, observed both and . Our manuscript will demonstrate the clinical significance of the complement system as a bridging figure between innate immunity and lipid homeostasis.

摘要

补体系统作为固有免疫应答的协调者和促进者,在维持宿主内环境稳定方面发挥着至关重要的作用。它促进病原体和危险相关分子模式的清除,调节适应性免疫,并可改变各种代谢过程,如能量消耗、脂质代谢和葡萄糖稳态。在本综述中,我们将聚焦于补体成分与脂质代谢之间复杂的相互作用。更确切地说,我们将展示补体系统激活和调节的改变如何影响脂质相关疾病(如动脉粥样硬化、肥胖、代谢综合征、年龄相关性黄斑变性和代谢功能障碍相关脂肪性肝病)的病理结局。除此之外,我们将呈现并评估所观察到的潜在补体介导的生理机制。我们的论文将证明补体系统作为固有免疫和脂质稳态之间的桥梁人物的临床意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c076/11614835/da9c5c3e4683/fimmu-15-1511886-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c076/11614835/da9c5c3e4683/fimmu-15-1511886-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c076/11614835/da9c5c3e4683/fimmu-15-1511886-g001.jpg

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The complement system in lipid-mediated pathologies.脂质介导的病理学中的补体系统。
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本文引用的文献

1
The Relationship between the complement system and subclinical carotid atherosclerosis in patients with rheumatoid arthritis.补体系统与类风湿关节炎患者亚临床颈动脉粥样硬化的关系。
Arthritis Res Ther. 2024 Jul 8;26(1):127. doi: 10.1186/s13075-024-03360-3.
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Canonical and non-canonical roles of complement in atherosclerosis.补体在动脉粥样硬化中的经典和非经典作用。
Nat Rev Cardiol. 2024 Nov;21(11):743-761. doi: 10.1038/s41569-024-01016-y. Epub 2024 Apr 10.
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High-Dimensional Single-Cell Multimodal Landscape of Human Carotid Atherosclerosis.
人类颈动脉粥样硬化的高维单细胞多模态图谱
Arterioscler Thromb Vasc Biol. 2024 Apr;44(4):930-945. doi: 10.1161/ATVBAHA.123.320524. Epub 2024 Feb 22.
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Intracellular C3 protects β-cells from IL-1β-driven cytotoxicity via interaction with Fyn-related kinase.细胞内 C3 通过与 Fyn 相关激酶相互作用,保护β细胞免受 IL-1β 驱动的细胞毒性。
Proc Natl Acad Sci U S A. 2024 Feb 20;121(8):e2312621121. doi: 10.1073/pnas.2312621121. Epub 2024 Feb 12.
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An integrative analysis of single-cell and bulk transcriptome and bidirectional mendelian randomization analysis identified C1Q as a novel stimulated risk gene for Atherosclerosis.单细胞和批量转录组的综合分析以及双向孟德尔随机化分析确定 C1Q 为动脉粥样硬化的一个新的刺激风险基因。
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The C5aR1 complement receptor: A novel immunomodulator of insulin action in skeletal muscle.C5aR1 补体受体:骨骼肌胰岛素作用的新型免疫调节剂。
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The complement system is linked to insulin resistance in patients with systemic lupus erythematosus.补体系统与系统性红斑狼疮患者的胰岛素抵抗有关。
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Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A State-of-the-Art Review.代谢功能障碍相关脂肪性肝病(MASLD):最新综述
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A guide to complement biology, pathology and therapeutic opportunity.补体生物学、病理学与治疗机会指南
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Cell-autonomous regulation of complement C3 by factor H limits macrophage efferocytosis and exacerbates atherosclerosis.补体因子 H 通过细胞自主调控补体 C3 限制巨噬细胞噬作用并加剧动脉粥样硬化。
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