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Extracellular vesicles in autoimmune diseases: Mechanistic underpinnings and precision medicine applications 自身免疫性疾病中的细胞外囊泡:机制基础和精准医学应用。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2025-11-21 DOI: 10.1016/j.autrev.2025.103959
Wenhui Mo , Yujie Zhang , Yu Zeng, Yanyi Zheng, Shenglan Zhao, Xiaoze Wang, Xiaoli Fan
Autoimmune diseases constitute a collection of complex disorders characterized by abnormal immune responses directed against self-tissues. The pathogenesis of these diseases is strongly linked to the interaction of genetic predispositions and environmental influences. Clinically, autoimmune diseases present with heterogeneous manifestations, and their prevalence has been steadily rising, resulting in profound impacts on patients' physical and psychological health and creating a growing challenge for healthcare infrastructures. At present, nonspecific immunosuppressants are the main treatment method, but this method has limitations such as extensive immunosuppression and serious adverse reactions. Therefore, there is an urgent need to develop novel and targeted therapeutic strategies. As crucial mediators of intercellular communication, extracellular vesicles (EVs) have become significant actors in the control of inflammatory and immunological responses, showing great promise in both mechanistic studies and clinical applications. This study offers a comprehensive overview of current developments in EV research for the main autoimmune conditions, including inflammatory bowel disease, systemic lupus erythematosus, and rheumatoid arthritis. It further comprehensively discusses the potential clinical value of EVs from the perspectives of disease pathogenesis and biomarker development, aiming to offer theoretical support and innovative directions for the clinical application of EV-based diagnostics and treatments, as well as for the realization of precision medicine in autoimmune disorders.
自身免疫性疾病是一种以针对自身组织的异常免疫反应为特征的复杂疾病的集合。这些疾病的发病机制与遗传倾向和环境影响的相互作用密切相关。在临床上,自身免疫性疾病表现各异,发病率稳步上升,对患者身心健康产生深远影响,对医疗卫生基础设施构成越来越大的挑战。目前,非特异性免疫抑制剂是主要的治疗方法,但这种方法存在广泛的免疫抑制和严重的不良反应等局限性。因此,迫切需要开发新的靶向治疗策略。作为细胞间通讯的重要介质,细胞外囊泡(EVs)已成为控制炎症和免疫反应的重要角色,在机制研究和临床应用中都显示出巨大的前景。本研究全面概述了目前EV在主要自身免疫性疾病(包括炎症性肠病、系统性红斑狼疮和类风湿性关节炎)中的研究进展。进一步从疾病发病机制和生物标志物开发等方面全面探讨ev潜在的临床价值,旨在为基于ev的诊断和治疗的临床应用,实现自身免疫性疾病的精准医疗提供理论支持和创新方向。
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引用次数: 0
Targeting age-related cell-free DNA for prevention, early diagnosis and treatment of rheumatoid arthritis 靶向年龄相关的无细胞DNA用于类风湿关节炎的预防、早期诊断和治疗。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2025-11-29 DOI: 10.1016/j.autrev.2025.103961
Ning Ma , Yulin Xu , Dingqi Zhang , Huan-Tian Zhang , Weidan Luo , Yang Cao , Vincent Kam Wai Wong
Cell-free DNA (cf-DNA) refers to extracellular DNA fragments released during cell death, which have been observed to accumulate with advancing age. Elevated cf-DNA concentrations have been detected in the plasma and disease-affected tissues of patients with multiple disorders, particularly age-related autoimmune diseases such as rheumatoid arthritis (RA). Growing evidence supports the potential of cf-DNA as a biomarker for a broad spectrum of autoimmune and age-associated conditions, including cancer, systemic lupus erythematosus (SLE), and psoriasis. Fluctuations in cf-DNA levels and characteristics appear to be closely associated with disease onset, progression, severity, and prognosis. Importantly, emerging studies indicate that cf-DNA may not merely act as a passive biomarker but could also function as an active mediator contributing to RA pathogenesis through distinct immunological pathways. These insights suggest that cf-DNA represents a promising target for the development of innovative diagnostic, preventive, and therapeutic strategies. In this review, we summarize the current understanding of age-related cf-DNA in RA, highlight its potential immunopathological roles, and discuss recent advances in cf-DNA–based diagnostic tools, preventive approaches, and therapeutic interventions with possible clinical translational value.
游离细胞DNA (cf-DNA)是指细胞死亡过程中释放的细胞外DNA片段,它们随着年龄的增长而积累。在患有多种疾病,特别是与年龄相关的自身免疫性疾病(如类风湿性关节炎)的患者的血浆和疾病影响组织中检测到升高的cf-DNA浓度。越来越多的证据支持cf-DNA作为广泛的自身免疫和年龄相关疾病的生物标志物的潜力,包括癌症、系统性红斑狼疮(SLE)和牛皮癣。cf-DNA水平和特征的波动似乎与疾病的发病、进展、严重程度和预后密切相关。重要的是,新出现的研究表明,cf-DNA可能不仅仅作为一种被动的生物标志物,还可以作为一种主动的介质,通过不同的免疫途径参与RA的发病机制。这些见解表明,cf-DNA代表了创新诊断、预防和治疗策略发展的一个有希望的目标。在这篇综述中,我们总结了目前对RA中年龄相关的cf-DNA的理解,强调了其潜在的免疫病理作用,并讨论了基于cf-DNA的诊断工具,预防方法和治疗干预的最新进展,可能具有临床转化价值。
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引用次数: 0
Discrepancy between international guidelines and global laboratory practices in autoantibody testing for autoimmune hepatitis 自身免疫性肝炎自身抗体检测国际指南与全球实验室实践的差异
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2025-12-06 DOI: 10.1016/j.autrev.2025.103973
Nicola Bizzaro , Dimitrios Bogdanos
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引用次数: 0
Metabolic traits of T cells and the implications in autoimmune diseases T细胞的代谢特性及其在自身免疫性疾病中的意义
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2026-01-22 DOI: 10.1016/j.autrev.2026.103989
Yi Zhou , Yuqi Zhou , Qing Zhu , Weinan Guo , Chunying Li
The metabolic activities of T cells play a pivotal role in regulating their activation, differentiation, and effector functions. In recent years, it has emerged as a key focus of research in the maintenance of immune homeostasis and the modulation of inflammatory responses. T cells not only rely on metabolic reprogramming to meet their energy and biosynthesis demands, but also utilize intermediate metabolites to regulate epigenetic modifications and then affect gene expression and cell fate. More importantly, T cell metabolism faces adaptive pressures in tissue-specific microenvironments, which impact their effector capabilities and participate in immune tolerance maintenance. Currently, traditional immunosuppressive therapy still has limitations in the treatment of autoimmune diseases, with notable side effects. Meanwhile, targeting T cell metabolism, as an emerging strategy for intervening in autoimmune responses, has demonstrated promising potential in multiple research studies. This review provides a comprehensive overview of the metabolic characteristics of T cells at different developmental stages and functional states, explores the interactive mechanisms between metabolism and epigenetic regulation in T cells, and discusses the influence of tissue microenvironments on T cell metabolic behavior. Finally, we highlighted recent advancements in targeting T cell metabolism for treating systemic lupus erythematosus, psoriasis, inflammatory bowel disease, and multiple sclerosis. This provides new directions for developing precise clinical intervention strategies for patients with autoimmune diseases.
T细胞的代谢活动在调节其激活、分化和效应功能中起着关键作用。近年来,它已成为免疫稳态维持和炎症反应调节的研究热点。T细胞不仅依靠代谢重编程来满足自身的能量和生物合成需求,还利用中间代谢物调节表观遗传修饰,进而影响基因表达和细胞命运。更重要的是,T细胞代谢在组织特异性微环境中面临适应性压力,这影响了它们的效应能力并参与免疫耐受维持。目前,传统的免疫抑制疗法在自身免疫性疾病的治疗中仍有局限性,且副作用明显。同时,靶向T细胞代谢作为一种干预自身免疫反应的新兴策略,在多项研究中显示出了良好的潜力。本文综述了T细胞在不同发育阶段和功能状态下的代谢特征,探讨了T细胞代谢与表观遗传调控之间的相互作用机制,并讨论了组织微环境对T细胞代谢行为的影响。最后,我们强调了靶向T细胞代谢治疗系统性红斑狼疮、牛皮癣、炎症性肠病和多发性硬化症的最新进展。这为自身免疫性疾病患者制定精准的临床干预策略提供了新的方向。
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引用次数: 0
The regulatory roles of Beta-2 glycoprotein I (β2GPI) in thrombosis and hemostasis and abnormal disease conditions developed by autoantibodies against β2GPI β -2糖蛋白I (β2GPI)在抗β2GPI自身抗体引起的血栓、止血和异常疾病状况中的调节作用
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2026-01-01 DOI: 10.1016/j.autrev.2025.103984
Ruiying Wang , Xian Wen Tan , Chunyan Yu , Min Li , Siyu Wang , Bingshu Yuan , Xiaoxuan Ma , Qingping Liu , Eiji Matsuura , Lianhua Shen
Beta-2 glycoprotein I (β2GPI) as a core target antigen of antiphospholipid antibodies (aPLs), is a multifunctional plasma protein with phospholipid-binding properties. Under physiological conditions, β2GPI not only binds to negatively charged phospholipids via its domain V but also interacts with various molecules, such as angiostatin4.5 (AS4.5) and annexin II. These interactions play key roles in maintaining the balance between procoagulant and anticoagulant processes and in promoting angiogenesis. β2GPI binds to pathophysiological ligands, such as apoptotic cells, oxidized low-density lipoprotein (oxLDL) and neutrophil extracellular traps (NETs). These complexes can trigger the production of anti-β2GPI autoantibodies in autoimmune patients, leading to antiphospholipid syndrome (APS). The resulting IgG immune complexes activate and impair endothelial cells, resulting in aberrant activation of the coagulation cascade, disruption of lipid metabolic homeostasis, and breakdown of immune tolerance. Together, these processes promote thrombotic events in APS and accelerate the progression of atherosclerotic plaques. This review paper summaries the dynamic conformational transitions of β2GPI's functional domains that elucidates the dual regulatory role of β2GPI-mediated molecular interactions in thrombosis and atherosclerosis (AS) and reveals the mechanism by which anti-β2GPI autoantibodies mediate endothelial injury, thrombosis, and inflammatory amplification. These findings may provide a theoretical molecular basis for the development of novel diagnostic and therapeutic strategies targeting β2GPI.

Take home message

  • β2GPI maintains the balance between procoagulant and anticoagulant processes and regulates angiogenesis.
  • Under pathological conditions, immune complexes of β2GPI with multiple molecules such as PS, oxLDL and PF4 drive the pathological cascade of endothelial damage-thrombosis-inflammatory amplification.
  • Dual-domain targeting (e.g., for stabilizing of DI-DV interaction) to mask antigenicity of β2GPI is potentially useful for inhibiting pathogenic antibody production.
β -2糖蛋白I (β2GPI)是一种具有磷脂结合特性的多功能血浆蛋白,是抗磷脂抗体(apis)的核心靶抗原。生理条件下,β2GPI不仅通过结构域V与带负电荷的磷脂结合,还可与多种分子相互作用,如angiostatin4.5 (AS4.5)和膜联蛋白II。这些相互作用在维持促凝和抗凝过程之间的平衡以及促进血管生成方面发挥着关键作用。β2GPI结合病理生理配体,如凋亡细胞、氧化低密度脂蛋白(oxLDL)和中性粒细胞胞外陷阱(NETs)。这些复合物可触发自身免疫性患者产生抗β 2gpi自身抗体,导致抗磷脂综合征(APS)。由此产生的IgG免疫复合物激活并损害内皮细胞,导致凝血级联异常激活,破坏脂质代谢稳态,破坏免疫耐受。总之,这些过程促进APS的血栓形成事件并加速动脉粥样硬化斑块的进展。本文综述了β2GPI功能域的动态构象转变,阐明了β2GPI介导的分子相互作用在血栓形成和动脉粥样硬化(AS)中的双重调节作用,揭示了抗β2GPI自身抗体介导内皮损伤、血栓形成和炎症放大的机制。这些发现可能为开发针对β2GPI的新型诊断和治疗策略提供理论分子基础。带回家的信息。
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引用次数: 0
The metabolic landscape of connective tissue diseases: Applications and discoveries in metabolomics research 结缔组织疾病的代谢景观:代谢组学研究中的应用和发现。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2025-12-08 DOI: 10.1016/j.autrev.2025.103975
Yinlan Wu , Daihua Deng , Yanhong Li , Sijun Zhang , Tong Wu , Deying Huang , Lu Cheng , Yi Liu , Chunyu Tan , Yubin Luo
Metabolomics has significantly advanced our understanding of connective tissue diseases (CTDs) in recent years by revealing the complex metabolic alterations that underlie these autoimmune disorders. This comprehensive review synthesizes current knowledge on how metabolomics elucidates CTDs pathogenesis, enhances diagnostic precision, and guides therapeutic interventions. Central to this discussion are pivotal metabolic pathways—including those of amino acids, lipids, and carbohydrates—which exhibit distinct dysregulation patterns across different CTDs. These metabolic shifts not only reflect disease activity and severity but also offer potential biomarkers for early detection and monitoring. Advanced metabolomic technologies have facilitated the identification of novel therapeutic targets by uncovering the metabolic networks that govern immune responses and inflammation. Furthermore, metabolomics bridges the gap between host metabolism and gut microbiota, shedding light on how microbial metabolites influence immune homeostasis and disease progression. The integration of metabolomics with other omics disciplines promises a more holistic understanding of CTDs, paving the way for personalized medicine. This review highlights the transformative potential of metabolomics in CTDs research, underscoring its role in uncovering the molecular mechanisms driving these diseases and inspiring innovative management and treatment strategies.
近年来,代谢组学通过揭示这些自身免疫性疾病背后的复杂代谢改变,显著提高了我们对结缔组织疾病(CTDs)的理解。这篇综述综合了代谢组学如何阐明CTDs发病机制、提高诊断精度和指导治疗干预的现有知识。这个讨论的核心是关键的代谢途径——包括氨基酸、脂质和碳水化合物——它们在不同的CTDs中表现出不同的失调模式。这些代谢变化不仅反映了疾病的活动性和严重程度,而且为早期发现和监测提供了潜在的生物标志物。先进的代谢组学技术通过揭示控制免疫反应和炎症的代谢网络,促进了新的治疗靶点的鉴定。此外,代谢组学弥补了宿主代谢和肠道微生物群之间的差距,揭示了微生物代谢物如何影响免疫稳态和疾病进展。代谢组学与其他组学学科的整合有望更全面地了解CTDs,为个性化医疗铺平道路。这篇综述强调了代谢组学在CTDs研究中的变革潜力,强调了它在揭示驱动这些疾病的分子机制和激发创新管理和治疗策略方面的作用。
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引用次数: 0
Therapeutic approaches in adults with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): A review of current evidence 髓鞘少突胶质细胞糖蛋白抗体相关疾病(MOGAD)成人的治疗方法:当前证据综述
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2025-12-02 DOI: 10.1016/j.autrev.2025.103970
Jakob Stögbauer , Victoria Schegerer , Clemens Klein , Marc Pawlitzki , Sven G. Meuth , Orhan Aktas , Sergiu Groppa , Mathias Fousse
Recent years have seen a considerable increase in knowledge pertaining to Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD). Nevertheless, a noteworthy degree of uncertainty remains within the neurological community, primarily due to the often highly heterogeneous nature of the disease and the absence of approved long-term treatment options. In this article, we undertake a comprehensive review of the various treatment strategies and drug options available for the pharmacological treatment of acute attacks and relapses in MOGAD.
近年来,有关髓鞘少突胶质细胞糖蛋白抗体相关疾病(MOGAD)的知识有了相当大的增加。然而,神经学界仍然存在很大程度的不确定性,这主要是由于该疾病往往具有高度异质性,并且缺乏经批准的长期治疗方案。在这篇文章中,我们对MOGAD急性发作和复发的各种治疗策略和药物选择进行了全面的回顾。
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引用次数: 0
LAG-3 in (auto)immunity and cancer - Emphasising its role in antigen presenting cells LAG-3在(自身)免疫和癌症中的作用——强调其在抗原呈递细胞中的作用。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2026-01-24 DOI: 10.1016/j.autrev.2026.103992
Aleksandra Wiśniewska , Elżbieta Sarnowska , Katarzyna Kozak , Piotr Rutkowski , Paweł Sobczuk
The growing popularity of immunotherapy shows a promising future for cancer treatment. However, a significant need to develop new therapeutics that could be successfully used in therapy still remains, especially in “immune-cold” tumors that are not responsive to classic anti-PD-1 treatment. Therefore, the discovery of lymphocyte activation gene-3 (LAG-3) as a new immune checkpoint (IC) molecule that physiologically participates in auto-tolerance mechanisms preventing auto-aggression was a significant milestone in immuno-oncology. Two main approaches aim to introduce LAG-3-directed therapies into clinical practice: anti-LAG-3 antibodies that are meant to inhibit LAG-3 function and recombinant soluble LAG-3 form that aim to activate immune response, especially by interacting with the antigen-presenting cells (APCs). So far, studies show that both approaches may be safe and effective anti-cancer treatment options. This review summarises the role of LAG-3 in immune response and emphasises the role of this IC molecule and its soluble form on APCs function, while also noting the primary physiological function of LAG-3 in autoimmunity and providing a dual perspective of the pros and cons of this novel anti-cancer therapy.
免疫疗法的日益普及显示出癌症治疗的良好前景。然而,仍然需要开发能够成功用于治疗的新疗法,特别是在对经典抗pd -1治疗无反应的“免疫冷”肿瘤中。因此,淋巴细胞活化基因-3 (LAG-3)作为一种新的免疫检查点(IC)分子的发现,在生理上参与了自身耐受机制,防止自身攻击,是免疫肿瘤学的一个重要里程碑。两种主要的方法旨在将LAG-3导向疗法引入临床实践:旨在抑制LAG-3功能的抗LAG-3抗体和旨在激活免疫反应的重组可溶性LAG-3形式,特别是通过与抗原呈递细胞(APCs)相互作用。到目前为止,研究表明这两种方法都可能是安全有效的抗癌治疗选择。本文综述了LAG-3在免疫应答中的作用,重点介绍了这种IC分子及其可溶形式在APCs功能中的作用,同时也指出了LAG-3在自身免疫中的主要生理功能,并对这种新型抗癌疗法的利弊进行了双重分析。
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引用次数: 0
Gastrointestinal histology of systemic sclerosis: A systematic review 系统性硬化症的胃肠组织学:系统综述。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-02-01 Epub Date: 2026-01-23 DOI: 10.1016/j.autrev.2026.103988
Aidan K. Strother , Robert M. Anderton , Naveen Kalavar , Ali Y. Ayla , Tracy Ashby , Amanda Mayer , Roshan Dongre , Francesco Bonomi , Silvia Bellando Randone , Michael Hughes , Zsuzsanna H. McMahan

Objective

To systematically review and synthesize the histological findings of gastrointestinal (GI) tissue in patients with systemic sclerosis (SSc), aiming to clarify the role of fibrosis and other pathological processes in SSc-related GI disease.

Methods

A comprehensive literature search was conducted across MEDLINE (OVID), Web of Science, and Cochrane Library databases for studies published in English from 1960 to 2025. Inclusion criteria required studies to report qualitative histological findings from GI tissue (esophagus to anorectum) in adult SSc patients, excluding those with overlapping autoimmune diseases or malignancy. Data extraction and appraisal were performed independently by multiple reviewers.

Results

Of 1697 screened articles, 36 met inclusion criteria. Histological analysis revealed that fibrosis, while common, was not universal nor evenly distributed across GI layers. The mucosa predominantly exhibited inflammatory infiltrates (mast cells, macrophages, lymphocytes), villous atrophy, and less frequent fibrosis. Submucosal findings were inconsistent, with variable reports of vascular changes and nerve plexus degeneration. The muscularis layer showed near-universal smooth muscle atrophy and variable fibrosis, with decreased density of interstitial cells of Cajal (ICC) in some studies. Neuronal and mitochondrial pathology were underreported.

Conclusion

GI pathology in SSc is multifaceted, involving inflammation, cellular degeneration, neuronal dysfunction, and smooth muscle atrophy, with fibrosis as a variable feature. Standardization of histological reporting and further ultrastructural studies are needed to elucidate mechanisms and guide future research and therapeutic strategies.
目的:系统回顾和综合系统性硬化症(SSc)患者胃肠道(GI)组织的组织学表现,旨在阐明纤维化等病理过程在SSc相关胃肠道疾病中的作用。方法:通过MEDLINE (OVID)、Web of Science和Cochrane Library数据库进行全面的文献检索,检索1960年至2025年发表的英文研究。纳入标准要求研究报告成人SSc患者胃肠道组织(食道至肛肠)的定性组织学发现,排除重叠自身免疫性疾病或恶性肿瘤。数据提取和评估由多位审稿人独立完成。结果:在1697篇筛选文章中,36篇符合纳入标准。组织学分析显示,纤维化虽然常见,但并不普遍,也不均匀分布于胃肠道各层。粘膜主要表现为炎症浸润(肥大细胞、巨噬细胞、淋巴细胞)、绒毛萎缩和较少发生的纤维化。粘膜下的发现不一致,有不同的血管改变和神经丛变性的报道。肌层表现为几乎普遍的平滑肌萎缩和变异性纤维化,部分研究显示Cajal间质细胞(ICC)密度降低。神经元和线粒体病理少报。结论:SSc的胃肠道病理是多方面的,包括炎症、细胞变性、神经元功能障碍和平滑肌萎缩,纤维化是一个可变的特征。需要组织报告的标准化和进一步的超微结构研究来阐明机制并指导未来的研究和治疗策略。
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引用次数: 0
Ferritinophagy in inflammatory and autoimmune diseases: Mechanistic insights and therapeutic potentials 炎症和自身免疫性疾病中的铁蛋白吞噬:机制见解和治疗潜力。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 Epub Date: 2025-10-30 DOI: 10.1016/j.autrev.2025.103954
Yi Wang , Yang Li , Jiani Jiang , Yanggang Hong , Sheng Gao , Chunyan Hua
Ferritinophagy, a selective form of autophagy mediated by nuclear receptor coactivator 4 (NCOA4), degrades ferritin to regulate intracellular iron homeostasis and has emerged as an important process in inflammatory and autoimmune diseases. By controlling ferritin turnover, ferritinophagy affects labile iron levels and ferroptosis, an iron-dependent cell death driven by lipid peroxidation, and interacts with multiple immune regulatory pathways. This process is modulated by signaling networks such as MAPK, cGAS-STING, NF-κB, AMPK/mTOR, and NRF2, which link iron metabolism to inflammatory responses. Aberrant ferritinophagy has been implicated in conditions including sepsis, osteoarthritis, asthma, rheumatoid arthritis, and systemic lupus erythematosus. Preclinical studies demonstrate that strategies such as inhibiting the JNK-JUN or cGAS-STING pathways, or applying iron chelators like deferoxamine, can reduce iron overload, limit ferroptosis, and attenuate inflammation. Despite these advances, further work is needed to delineate disease-specific regulatory mechanisms and to translate ferritinophagy modulation into safe and effective therapies. This review summarizes current mechanistic insights and therapeutic prospects, highlighting ferritinophagy as a promising target for managing inflammatory and autoimmune disorders.
铁蛋白自噬是一种选择性的自噬形式,由核受体共激活因子4 (NCOA4)介导,降解铁蛋白调节细胞内铁稳态,已成为炎症和自身免疫性疾病的重要过程。通过控制铁蛋白周转,铁蛋白自噬影响不稳定的铁水平和铁凋亡,铁凋亡是一种由脂质过氧化驱动的铁依赖性细胞死亡,并与多种免疫调节途径相互作用。这一过程由信号网络调控,如MAPK、cGAS-STING、NF-κB、AMPK/mTOR和NRF2,它们将铁代谢与炎症反应联系起来。异常的铁蛋白吞噬与脓毒症、骨关节炎、哮喘、类风湿关节炎和系统性红斑狼疮等疾病有关。临床前研究表明,抑制JNK-JUN或cGAS-STING通路,或应用铁螯合剂如去铁胺,可以减少铁过载,限制铁下垂,减轻炎症。尽管取得了这些进展,但需要进一步的工作来描述疾病特异性调节机制,并将铁蛋白吞噬调节转化为安全有效的治疗方法。这篇综述总结了目前的机制见解和治疗前景,强调了铁蛋白噬作为治疗炎症和自身免疫性疾病的有希望的靶点。
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引用次数: 0
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Autoimmunity reviews
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