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免疫代谢、细胞外囊泡与心脏损伤。

Immunometabolism, extracellular vesicles and cardiac injury.

机构信息

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, United States.

出版信息

Front Endocrinol (Lausanne). 2024 Jan 8;14:1331284. doi: 10.3389/fendo.2023.1331284. eCollection 2023.

DOI:10.3389/fendo.2023.1331284
PMID:38260141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10800986/
Abstract

Recent evidence from our lab and others suggests that metabolic reprogramming of immune cells drives changes in immune cell phenotypes along the inflammatory-to-reparative spectrum and plays a critical role in mediating the inflammatory responses to cardiac injury (e.g. hypertension, myocardial infarction). However, the factors that drive metabolic reprogramming in immune cells are not fully understood. Extracellular vesicles (EVs) are recognized for their ability to transfer cargo such as microRNAs from remote sites to influence cardiac remodeling. Furthermore, conditions such as obesity and metabolic syndrome, which are implicated in the majority of cardiovascular disease (CVD) cases, can skew production of EVs toward pro-inflammatory phenotypes. In this mini-review, we discuss the mechanisms by which EVs may influence immune cell metabolism during cardiac injury and factors associated with obesity and the metabolic syndrome that can disrupt normal EV function. We also discuss potential sources of cardio-protective and anti-inflammatory EVs, such as brown adipose tissue. Finally, we discuss implications for future therapeutics.

摘要

最近我们实验室和其他实验室的证据表明,免疫细胞的代谢重编程沿着炎症到修复的谱系驱动免疫细胞表型的变化,并在介导心脏损伤(例如高血压、心肌梗死)的炎症反应中发挥关键作用。然而,驱动免疫细胞代谢重编程的因素尚不完全清楚。细胞外囊泡(EVs)因其能够将货物(如 microRNA)从远处转移到影响心脏重构的能力而受到关注。此外,肥胖和代谢综合征等与大多数心血管疾病(CVD)病例有关的情况,会使 EV 的产生偏向促炎表型。在这篇迷你综述中,我们讨论了 EVs 可能在心脏损伤期间影响免疫细胞代谢的机制,以及与肥胖和代谢综合征相关的因素,这些因素会破坏正常 EV 的功能。我们还讨论了潜在的心脏保护和抗炎性 EV 来源,如棕色脂肪组织。最后,我们讨论了对未来治疗的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcd1/10800986/120dd92a17cf/fendo-14-1331284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcd1/10800986/120dd92a17cf/fendo-14-1331284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcd1/10800986/120dd92a17cf/fendo-14-1331284-g001.jpg

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本文引用的文献

1
Cardiac macrophages and emerging roles for their metabolism after myocardial infarction.心肌梗死后心脏巨噬细胞及其代谢的新作用。
J Clin Invest. 2023 Sep 15;133(18):e171953. doi: 10.1172/JCI171953.
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Immunometabolism at the Heart of Cardiovascular Disease.免疫代谢是心血管疾病的核心
JACC Basic Transl Sci. 2023 Apr 26;8(7):884-904. doi: 10.1016/j.jacbts.2022.12.010. eCollection 2023 Jul.
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MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.MicroRNA-22 通过靶向 GLUT1 和 4-1BBL 调节巨噬细胞的促炎反应和 M1 极化。
代谢综合征治疗的研究进展
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Temporal changes in glucose metabolism reflect polarization in resident and monocyte-derived macrophages after myocardial infarction.心肌梗死后葡萄糖代谢的时间变化反映了驻留巨噬细胞和单核细胞衍生巨噬细胞的极化。
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The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.细胞外囊泡与炎症相关疾病中线粒体的复杂关联
Int J Mol Sci. 2023 May 3;24(9):8181. doi: 10.3390/ijms24098181.
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The Potential Use of Mitochondrial Extracellular Vesicles as Biomarkers or Therapeutical Tools.线粒体细胞外囊泡作为生物标志物或治疗工具的潜在用途。
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