腹主动脉瘤中的髓样细胞。

IF 5.7 2区 医学 Q1 PERIPHERAL VASCULAR DISEASE
Wen-Tao Yang, Fang-Da Li, Yue-Hong Zheng, Lei Wang
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引用次数: 0

摘要

回顾目的:腹主动脉瘤(AAA)是一种危及生命的血管疾病,破裂后死亡率高,但有效的药物治疗仍然缺乏。本文综述了髓系细胞(主动脉炎症和重塑的关键介质)在AAA发病机制中的关键作用,并强调了它们的治疗靶向潜力。最近发现:单细胞RNA测序揭示了AAA的髓系多样性。在这些髓系群体中,巨噬细胞(包括干扰素应答单核细胞、促炎性和抗炎亚群以及修复性群体)成为AAA发病机制的中心调节因子,影响疾病的发生、进展和组织修复过程。中性粒细胞通过中性粒细胞胞外陷阱促进血管损伤,而树突状细胞则架起先天适应性免疫的桥梁。嗜酸性粒细胞和髓源性抑制细胞表现出免疫调节的保护作用。机制研究确定了髓细胞可塑性的转录、代谢和表观遗传调节因子。克隆造血和训练免疫可能是髓细胞参与AAA的潜在新机制。这些机制见解激发了治疗创新,纳米颗粒靶向髓细胞治疗在缓解AAA进展方面显示出有希望的免疫调节作用。髓系细胞通过驱动炎症反应、细胞外基质降解和血管重构失调,在AAA发病机制中起关键作用。它们的功能异质性,包括破坏性和保护性亚群,强调了精确靶向治疗方法的必要性。虽然单细胞技术极大地促进了我们对骨髓多样性的理解,但临床翻译仍然受到微环境串扰和潜在脱靶效应的挑战。未来的研究应优先考虑:(1)骨髓-血管相互作用的空间多组学表征;(2)针对克隆造血驱动亚群的精确治疗开发;(3)重新编程致病性骨髓表型的组合策略。解决这些关键的空白可能会导致动脉瘤稳定的变革性治疗,最终满足AAA级临床管理的迫切需求。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myeloid Cells in Abdominal Aortic Aneurysm.

Purpose of review: Abdominal aortic aneurysm (AAA) is a life-threatening vascular disorder with high mortality upon rupture, yet effective pharmacotherapy remains lacking. This review synthesizes the pivotal roles of myeloid cells-key mediators of aortic inflammation and remodeling-in AAA pathogenesis, highlighting their therapeutic targeting potential.

Recent findings: Single-cell RNA sequencing has revealed myeloid diversity in AAA. Among these myeloid populations, macrophages (including interferon-responsive monocytes, pro- and anti-inflammatory subsets, and reparative populations) emerge as central regulators of AAA pathogenesis, influencing disease initiation, progression, and tissue repair processes. Neutrophils promote vascular injury via neutrophil extracellular traps, while dendritic cells bridge innate-adaptive immunity. Eosinophils and myeloid-derived suppressor cells exhibited protective effects by immunoregulation. Mechanistic studies identified transcriptional, metabolic, and epigenetic regulators of myeloid plasticity. Clonal hematopoiesis and trained immunity may serve as potential novel mechanisms of myeloid cells involved in AAA. These mechanistic insights have inspired therapeutic innovation, with nanoparticle-targeted myeloid cell therapies showing promising immunomodulatory effects in mitigating AAA progression. Myeloid cells play a pivotal role in AAA pathogenesis by driving inflammatory responses, extracellular matrix degradation, and maladaptive vascular remodeling. Their functional heterogeneity, encompassing both destructive and protective subsets, highlights the need for precisely targeted therapeutic approaches. While single-cell technologies have significantly advanced our understanding of myeloid diversity, clinical translation remains challenged by microenvironmental crosstalk and potential off-target effects. Future research should prioritize: (1) spatial multi-omics characterization of myeloid-vascular interactions, (2) development of precision therapies targeting clonal hematopoiesis-driven subpopulations, and (3) combinatorial strategies to reprogram pathogenic myeloid phenotypes. Addressing these critical gaps may lead to transformative therapies for aneurysm stabilization, ultimately fulfilling the urgent unmet needs in AAA clinical management.

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来源期刊
CiteScore
9.00
自引率
3.40%
发文量
87
审稿时长
6-12 weeks
期刊介绍: The aim of this journal is to systematically provide expert views on current basic science and clinical advances in the field of atherosclerosis and highlight the most important developments likely to transform the field of cardiovascular prevention, diagnosis, and treatment. We accomplish this aim by appointing major authorities to serve as Section Editors who select leading experts from around the world to provide definitive reviews on key topics and papers published in the past year. We also provide supplementary reviews and commentaries from well-known figures in the field. An Editorial Board of internationally diverse members suggests topics of special interest to their country/region and ensures that topics are current and include emerging research.
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