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MTHFR polymorphisms in autoimmune diseases: Mechanistic and clinical perspectives 自身免疫性疾病中的MTHFR多态性:机制和临床观点。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103939
Ting Sun , Yuxian Wu , Lingyun Kong , Jingtong Wang , Feng Zhang , Yang Liu , Jie Gao , Yaoyang Liu
The methylenetetrahydrofolate reductase (MTHFR) gene encodes a crucial enzyme in folate metabolism, serving as a central regulator of homocysteine homeostasis and one‑carbon metabolic pathways. This review synthesizes current evidence on the mechanistic and clinical implications of two common MTHFR polymorphisms, C677T and A1298C, in autoimmune pathogenesis. We critically examine their contributions to inflammatory responses, endothelial dysfunction, immune imbalance, and epigenetic modifications. Furthermore, we analyze population-specific associations between these variants and susceptibility to eight autoimmune disorders, genotype-phenotype correlations related to clinical manifestations and comorbidities, as well as pharmacogenomic interactions influencing response to methotrexate therapy. By integrating genetic, molecular, and clinical insights, this review highlights the translational potential of MTHFR genotyping for improving risk stratification and personalized treatment strategies in autoimmune and immune-mediated inflammatory conditions.
亚甲基四氢叶酸还原酶(MTHFR)基因编码叶酸代谢中的一种关键酶,作为同型半胱氨酸稳态和单碳代谢途径的中心调节因子。本文综述了目前关于两种常见MTHFR多态性C677T和A1298C在自身免疫发病机制中的机制和临床意义的证据。我们严格检查他们的贡献炎症反应,内皮功能障碍,免疫失衡和表观遗传修饰。此外,我们分析了这些变异与8种自身免疫性疾病易感性之间的人群特异性关联,与临床表现和合并症相关的基因型-表型相关性,以及影响对甲氨蝶呤治疗反应的药物基因组学相互作用。通过整合遗传、分子和临床见解,本综述强调了MTHFR基因分型在改善自身免疫性和免疫介导性炎症的风险分层和个性化治疗策略方面的转化潜力。
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引用次数: 0
Immune checkpoint inhibitor-induced inflammatory arthritis vs rheumatoid arthritis: A comparative review 免疫检查点抑制剂诱导的炎性关节炎与类风湿关节炎:比较回顾。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103943
Iliopoulos Georgios , Sideridou Fani , Bogdanos Dmitrios , Liew David , Daoussis Dimitrios
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are frequently accompanied by immune-related adverse events (irAEs). Among these, ICI-induced inflammatory arthritis (ICI-IA) has emerged as the most common musculoskeletal toxicity, often mimicking rheumatoid arthritis (RA) in its clinical and imaging features. This narrative review synthesizes current evidence comparing ICI-IA with RA across epidemiology, pathophysiology, clinical presentation, imaging, treatment, and prognosis. While both entities share overlapping manifestations such as polyarthritis, synovitis, and joint erosions, ICI-IA is typically seronegative, arises subacutely after ICI initiation, and exhibits distinct immunopathologic signatures, including cytotoxic CD8+ T-cell predominance and unique B-cell alterations. ICI-IA may persist after ICI cessation, with chronic disease linked to improved oncologic outcomes. Therapeutic strategies require balancing arthritis control and preservation of anti-tumor immunity. Glucocorticoids and conventional disease modifying anti-rheumatic drugs (cDMARDs) are key players with proven safety and efficacy, whereas biologic therapies remain reserved for severe or refractory cases mainly due to cancer progression concerns. Furthermore, early rheumatology referral improves patient outcomes and reduces glucocorticoid exposure. Understanding the differences between ICI-IA and RA is essential for optimizing diagnosis, guiding individualized approach and applying precision medicine at the crossroads of oncology and rheumatology.
免疫检查点抑制剂(ICIs)已经改变了肿瘤的治疗前景,但经常伴随着免疫相关不良事件(irAEs)。其中,ici诱导的炎症性关节炎(ICI-IA)已成为最常见的肌肉骨骼毒性,其临床和影像学特征通常与类风湿关节炎(RA)相似。本文综述了ICI-IA与RA在流行病学、病理生理学、临床表现、影像学、治疗和预后方面的比较证据。虽然这两种疾病有重叠的表现,如多关节炎、滑膜炎和关节糜坏,但ICI- ia通常是血清阴性的,在ICI开始后亚急性出现,并表现出独特的免疫病理特征,包括细胞毒性CD8+ t细胞优势和独特的b细胞改变。ICI- ia可能在ICI停止后持续存在,慢性疾病与肿瘤预后改善有关。治疗策略需要平衡关节炎控制和保持抗肿瘤免疫。糖皮质激素和常规疾病修饰抗风湿药物(cDMARDs)是安全性和有效性被证明的关键因素,而生物疗法仍然保留用于严重或难治性病例,主要是由于癌症进展的担忧。此外,早期风湿病转诊可改善患者预后并减少糖皮质激素暴露。了解ICI-IA和RA之间的差异对于优化诊断、指导个体化治疗以及在肿瘤学和风湿病学交叉领域应用精准医学至关重要。
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引用次数: 0
VE/VCO2 at ventilatory threshold and peak VO2 in CPET studies of patients with scleroderma-associated PAH: A systematic review and meta-analyses 硬皮病相关PAH患者的CPET研究中通气阈值的VE/VCO2和峰值VO2:系统回顾和荟萃分析
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103942
Julie Better , Sylvie Leroy , Maarten K. Ninaber , Georgia Trakada , Bilge Kesikburun , Stephan Rosenkranz , Ralph Ewert , Dirk Habedank , Daniel Dumitrescu , Yanis Kouchit , Nihal Martis

Context

Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in patients with systemic sclerosis (SSc). Cardiopulmonary exercise testing (CPET) has been studied to detect SSc-associated PAH.

Objectives

To evaluate the diagnostic value of the ventilatory equivalent for CO2 at anaerobic or ventilatory threshold [VE/VCO2(VeT)] and peak oxygen uptake (peak VO2) for SSc-associated PAH obtained by CPET.

Methods

A systematic database search from 1993 to 2024 and meta-analyses were performed according to PRISMA guidelines to include original studies relating to SSc and CPET reporting VE/VCO2(VeT) and peak VO2. The random-effects model was chosen for the meta-analyses studying VE/VCO2(VeT), indexed and predicted percentage (%pred.) peak VO2, respectively. Meta-regression was only performed for VE/VCO2(VeT) with covariates defined as the percentage of limited cutaneous disease, percentage of interstitial lung disease, and %pred. of peak VO2.

Results

Out of 206 studies, 941 SSc patients from 15 studies were included. VE/VCO2(VeT) (11 studies, n = 850) was statistically lower in patients without PAH (32.68 ± 5.42 vs. 39.81 ± 9.32) with a mean effect size of −1.182 (95 %CI, −1.691 to −0.672; p < 0.001) (I2 = 86 %). The mean effect size for weight-indexed peak VO2 (11 studies, n = 848) was 0.713 (95 %CI, 0.371 to 1.054; p < 0.001) with higher values in patients without PAH (16.47 ± 4.62 vs. 13.61 ± 4.16 mL/kg/mn) (I2 = 70 %). Similarly, the mean effect size for %pred. Peak VO2 (12 studies, n = 850) was 0.659 (95 %CI, 0.425 to 0.894; p < 0.001) reflecting higher values in patients without PAH (74.00 ± 17.50 vs. 54.84 ± 18.14 %pred.) (I2 = 37 %). Meta-regression analysis of data from 7 studies did not yield significant p values for the covariates.

Conclusions

The effect size of each meta-analysis indicates that higher VE/VCO2(VeT) and lower peak VO2 may be considered as independent CPET markers of PAH in patients with SSc. CPET is a non-invasive and safe procedure for exploring dyspnoea in patients with SSc and, in association with conventional imaging techniques, may provide a reliable assessment of the presence of PAH.
背景:肺动脉高压(PAH)是系统性硬化症(SSc)患者死亡的主要原因之一。心肺运动试验(CPET)已被研究用于检测ssc相关的PAH。目的:评价CPET获得的无氧或通气阈值CO2通气当量[VE/VCO2(VeT)]和摄氧量峰值(VO2峰值)对ssc相关性PAH的诊断价值。方法:对1993 - 2024年的数据库进行系统检索,并根据PRISMA指南进行meta分析,纳入与SSc和CPET报告的VE/VCO2(VeT)和峰值VO2相关的原始研究。随机效应模型分别用于研究VE/VCO2(VeT)、指数和预测百分比(%pred.)峰值VO2的meta分析。仅对VE/VCO2(VeT)进行meta回归,协变量定义为局限性皮肤病百分比、间质性肺疾病百分比和pred %。VO2的峰值。结果:在206项研究中,纳入了来自15项研究的941例SSc患者。VE / VCO2(兽医)(11个研究中,n = 850)在统计学上低的病人没有多环芳烃(32.68 ±  5.42和39.81±9.32 )平均效应值为-1.182(95 % CI, -1.691 - -0.672; p 2 = 86 %)。体重指数峰值VO2的平均效应大小(11项研究,n = 848)为0.713(95 %CI, 0.371 ~ 1.054; p 2 = 70 %)。同样,%pred的平均效应大小。峰值VO2(12项研究,n = 850)为0.659(95 %CI, 0.425 ~ 0.894; p 2 = 37 %)。对7项研究的数据进行meta回归分析,协变量的p值均不显著。结论:各荟萃分析的效应大小表明,较高的VE/VCO2(VeT)和较低的峰值VO2可被视为SSc患者PAH的独立CPET标志物。CPET是一种无创、安全的检查SSc患者呼吸困难的方法,与常规成像技术相结合,可以可靠地评估PAH的存在。
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引用次数: 0
Environmental toxins and toxic metals in autoimmune diseases: Sex differences, hormonal influences, and immune dysregulation 自身免疫性疾病中的环境毒素和有毒金属:性别差异、激素影响和免疫失调。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103955
Geir Bjørklund , David R. Wallace , Kimiya Kangarlou , Fahimida Hossain , Massimiliano Peana
Environmental toxins, including toxic metal(oid)s such as mercury, lead, cadmium, and arsenic, as well as endocrine-disrupting chemicals like bisphenol A and phthalates, play a critical role in the onset and progression of autoimmune diseases. These substances accumulate in biological tissues and disrupt immune homeostasis through oxidative stress, molecular mimicry, and epigenetic modifications, mechanisms that contribute to autoantibody production and chronic inflammation, hallmarks of autoimmunity. Women are disproportionately affected by autoimmune diseases due to inherent differences in immune function, hormonal regulation, and genetic susceptibility. Estrogen, a key immunomodulatory hormone, can amplify immune responses and promote autoantibody generation. Its interaction with environmental toxins further exacerbates immune dysregulation, increasing female vulnerability to conditions such as systemic lupus erythematosus, rheumatoid arthritis, and autoimmune thyroid disorders. Hormonal fluctuations during puberty, pregnancy, and menopause additionally influence toxin metabolism and detoxification efficiency, compounding the risk of immune imbalance and disease onset in women. This review synthesizes current evidence on the mechanisms through which environmental toxicants contribute to autoimmune pathogenesis, with particular focus on sex-specific vulnerabilities. It explores the role of hormonal-immune-environment interactions across the female lifespan and highlights emerging research on epigenetic inheritance, gut dysbiosis, and biomarker development. By integrating mechanistic, epidemiological, and clinical findings, this review aims to inform targeted strategies for prevention, early detection, and risk reduction of environmentally driven autoimmune diseases.
环境毒素,包括有毒金属(类),如汞、铅、镉和砷,以及内分泌干扰化学物质,如双酚A和邻苯二甲酸盐,在自身免疫性疾病的发生和发展中起着关键作用。这些物质在生物组织中积累,通过氧化应激、分子模仿和表观遗传修饰破坏免疫稳态,这些机制有助于自身抗体的产生和慢性炎症,这是自身免疫的标志。由于免疫功能、激素调节和遗传易感性的固有差异,妇女受到自身免疫性疾病的影响不成比例。雌激素是一种重要的免疫调节激素,可以增强免疫反应,促进自身抗体的产生。它与环境毒素的相互作用进一步加剧了免疫失调,增加了女性对系统性红斑狼疮、类风湿性关节炎和自身免疫性甲状腺疾病等疾病的易感性。青春期、孕期和更年期的荷尔蒙波动还会影响毒素代谢和解毒效率,增加女性免疫失衡和发病的风险。这篇综述综合了目前关于环境毒物促进自身免疫发病机制的证据,特别关注性别特异性脆弱性。它探讨了激素-免疫-环境相互作用在女性生命周期中的作用,并重点介绍了表观遗传、肠道生态失调和生物标志物发育方面的新兴研究。通过整合机制、流行病学和临床研究结果,本综述旨在为环境驱动型自身免疫性疾病的预防、早期发现和降低风险提供有针对性的策略。
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引用次数: 0
The Trm-Treg Axis as a tissue-encoded immune checkpoint in chronic inflammation and autoimmunity Trm-Treg轴在慢性炎症和自身免疫中的组织编码免疫检查点作用
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-24 DOI: 10.1016/j.autrev.2025.103977
Liang Li , Yumin Xia , Yale Liu
Tissue-resident memory T (Trm) cells, once heralded as gatekeepers of localized immune protection, have emerged as central players in the pathogenesis of chronic inflammation and autoimmunity at epithelial barriers. At the heart of this immunological paradox lies the dynamic interplay between Trm and regulatory T (Treg) cells—a tissue-encoded checkpoint that calibrates immune defense against the need for tolerance and repair. Disruption of this axis unleashes the latent pathogenicity of Trm cells, fueling persistent inflammation, epithelial dysfunction, and disease relapse. Here, we propose that the Trm-Treg interaction acts as a molecular rheostat that tunes immune homeostasis at barrier sites. We dissect the tissue-specific mechanisms that sustain this alliance, highlight its failure in diseases such as inflammatory bowel disease (IBD), psoriasis, and chronic obstructive pulmonary disease (COPD), and explore emerging therapeutic strategies aimed at recalibrating this immune checkpoint to restore durable epithelial tolerance.
组织常驻记忆T (Trm)细胞,曾经被认为是局部免疫保护的守门人,已经成为慢性炎症和上皮屏障自身免疫发病机制的核心参与者。这一免疫学悖论的核心在于Trm和调节性T细胞(Treg)之间的动态相互作用。Treg是一种组织编码的检查点,校准免疫防御对耐受和修复的需求。这条轴的破坏释放了Trm细胞的潜伏致病性,助长了持续的炎症、上皮功能障碍和疾病复发。在这里,我们提出Trm-Treg相互作用作为一种分子变阻器,调节屏障部位的免疫稳态。我们剖析了维持这种联盟的组织特异性机制,强调了其在炎症性肠病(IBD)、牛皮癣和慢性阻塞性肺疾病(COPD)等疾病中的失败,并探索了旨在重新校准这种免疫检查点以恢复持久上皮耐受的新兴治疗策略。
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引用次数: 0
The role of sleep in multiple sclerosis. 睡眠在多发性硬化症中的作用。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-28 Epub Date: 2025-08-06 DOI: 10.1016/j.autrev.2025.103902
Susanna Cordone, Valentina Alfonsi, Luigi De Gennaro

Multiple Sclerosis (MS) is an autoimmunity-related disorder that mainly affects young adults. The high prevalence of the disease and its impact on patients' quality of life led researchers to investigate the etiopathogenesis of the disease to identify possible modifiable factors and consequent effective intervention strategies. Recent hypotheses suggest that the etiopathogenesis of MS is multifactorial and includes factors related to the immune system, neuroinflammation and neurodegeneration. In this scenario, sleep seems to have a close indirect relationship with MS, through its relationship with each of those factors and given the high incidence of sleep disorders in the MS population. Furthermore, given the growing interest of research in the mechanisms underlying MS and therapies able to alleviate MS-related symptoms at all stages of the disease, a more in-depth study of the role of sleep and its loss and disturbances and the factors intrinsically related to sleep and MS could be useful both to investigate the etiopathogenetic factors of MS and to develop non-invasive intervention strategies for MS treatment.

多发性硬化症(MS)是一种主要影响年轻人的自身免疫相关疾病。该疾病的高患病率及其对患者生活质量的影响促使研究人员调查该疾病的发病机制,以确定可能的可改变因素和随之而来的有效干预策略。最近的假设认为MS的发病是多因素的,包括与免疫系统、神经炎症和神经变性有关的因素。在这种情况下,睡眠似乎与多发性硬化症有密切的间接关系,通过它与这些因素的关系,并考虑到多发性硬化症人群中睡眠障碍的高发病率。此外,鉴于人们对多发性硬化症的发病机制和治疗方法的研究兴趣日益浓厚,对睡眠的作用、睡眠的丧失和障碍以及与睡眠和多发性硬化症内在相关的因素进行更深入的研究,可能有助于研究多发性硬化症的发病因素,并为多发性硬化症的治疗制定非侵入性干预策略。
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引用次数: 0
Adjusting fragility metrics for unequal trial randomizations 调整不平等试验随机化的脆弱性指标。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-09-17 DOI: 10.1016/j.autrev.2025.103935
Thomas F. Heston
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引用次数: 0
The effect of Sphingosine-1-phosphate receptor modulator treatment on leukocyte subsets across different clinical indications: A systematic review 鞘氨醇-1-磷酸受体调节剂治疗对不同临床适应症白细胞亚群的影响:一项系统综述。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-09-10 DOI: 10.1016/j.autrev.2025.103934
Dimitrios Nikolakis , Christoph Teichert , Joep Grootjans , Marleen G.H. van de Sande , Geert R. D’Haens

Background

Sphingosine-1-phosphate receptor (S1PR) modulators are approved as a treatment for several autoimmune diseases. While their role on total leukocyte populations is well-studied, their effects on specific leukocyte subsets remain unclear. This systematic review describes the impact of various S1PR modulators on human leukocyte subpopulations.

Methods

We conducted a systematic literature search through the databases PubMed, Medline, Embase, and Cochrane, up to the 25th of July 2024. Studies were included if they involved patients treated with S1PR modulators and provided data on leukocyte subsets. Among the exclusion criteria, were non-English articles, animal studies, and in vitro studies. Data extraction focused on changes in leukocyte subsets post-treatment.

Results

Out of 1658 articles identified, 63 met the inclusion criteria. Fingolimod was the most frequently studied agent and displayed significant reductions in total T-cell counts. More specifically, CD4+ T-cells, including naïve and central memory populations were reduced. CD8+ T-cells also decreased, although the alterations of effector memory subsets were inconsistent. B-lymphocytes were generally attenuated. Innate immune cells showed variable responses, with most studies indicating a reduction or no change. Data on other S1PR modulators suggested similar trends.

Conclusion

S1PR modulators primarily reduce T- and B-cell subpopulations, which are known to play a prominent role in immune-mediated inflammatory disorders. Further research is needed to fully elucidate the differential effects among drugs targeting specific isoforms of the S1PR, focusing on the lymph nodes or inflammatory tissue sites (e.g. intestinal mucosa and cerebrospinal fluid), to explore the exact clinical implications of these pharmacodynamic findings.
背景:鞘氨醇-1-磷酸受体(S1PR)调节剂已被批准用于治疗多种自身免疫性疾病。虽然它们对总白细胞群的作用已被充分研究,但它们对特定白细胞亚群的影响仍不清楚。这篇系统综述描述了各种S1PR调节剂对人类白细胞亚群的影响。方法:通过PubMed、Medline、Embase和Cochrane数据库进行系统的文献检索,检索时间截止到2024年7月25日。如果研究涉及接受S1PR调节剂治疗的患者并提供白细胞亚群数据,则纳入研究。排除标准包括非英文文章、动物研究和体外研究。数据提取的重点是治疗后白细胞亚群的变化。结果:1658篇文献中,63篇符合纳入标准。芬戈莫德是最常被研究的药物,并显示出总t细胞计数的显著减少。更具体地说,CD4+ t细胞,包括naïve和中枢记忆群减少。CD8+ t细胞也减少,尽管效应记忆亚群的改变不一致。b淋巴细胞普遍减弱。先天免疫细胞表现出不同的反应,大多数研究表明减少或没有变化。其他S1PR调制器的数据也显示了类似的趋势。结论:S1PR调节剂主要减少T细胞和b细胞亚群,这两种细胞在免疫介导的炎症疾病中起着重要作用。需要进一步的研究来充分阐明针对S1PR特定亚型的药物之间的差异效应,重点是淋巴结或炎症组织部位(如肠粘膜和脑脊液),以探索这些药效学发现的确切临床意义。
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引用次数: 0
Exploring therapeutic potential of Cannabis based therapy in autoimmune and rheumatic disorders 探索大麻治疗自身免疫性疾病和风湿病的治疗潜力。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-09-02 DOI: 10.1016/j.autrev.2025.103925
Inbar Michaeli , Simon Lassman , Gilad Halpert , Giris Jacob , Howard Amital
The medical use of cannabis is expanding across many countries, with some legalizing its use outright and others implementing medical licensure systems to approve treatment for eligible patients.
Despite this growing interest and utilization, there remains a lack of solid scientific evidence supporting its medical use, even though cannabis has been used therapeutically for thousands of years.
The goal of the following communication is to present updated data on the potential roles of cannabis-based treatments in various autoimmune and rheumatic conditions. The information highlights that incorporating cannabis into the therapeutic armamentarium may offer benefits. However, in many cases, despite encouraging perspectives and outcomes, the supporting evidence remains insufficient and requires further validation.
Due to social and legal barriers, the conduct of such rigorous clinical trials has been hindered, limiting the availability of high-quality evidence to guide medical practice.
大麻的医疗用途正在许多国家扩大,一些国家将其使用完全合法化,另一些国家实施医疗执照制度,批准对符合条件的患者进行治疗。尽管人们对大麻的兴趣和利用日益增加,但尽管大麻用于治疗已有数千年的历史,但仍然缺乏支持其医疗用途的可靠科学证据。以下通讯的目的是提供关于大麻治疗在各种自身免疫性和风湿病中的潜在作用的最新数据。该信息强调,将大麻纳入治疗手段可能会带来好处。然而,在许多情况下,尽管观点和结果令人鼓舞,但支持性证据仍然不足,需要进一步验证。由于社会和法律障碍,这种严格的临床试验的进行受到阻碍,限制了指导医疗实践的高质量证据的获得。
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引用次数: 0
Calcium signaling dysregulation in rheumatoid arthritis: a comparative perspective with osteoarthritis 类风湿关节炎中的钙信号失调:与骨关节炎的比较
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-08-28 DOI: 10.1016/j.autrev.2025.103923
Thuy Duong Nguyen , Hugo Abreu , Nicoletta Tommasi , Luigi Azzarone , Rita Maria Concetta Di Martino , Beatrice Riva , Davide Raineri , Tracey Pirali , Annalisa Chiocchetti , Giuseppe Cappellano
Rheumatoid arthritis and osteoarthritis are among the most prevalent chronic diseases worldwide, imposing a significant burden on both patients and healthcare systems. Despite their distinct etiology and progression, emerging evidence suggests that calcium signaling plays a pivotal role in the pathogenesis of both diseases by influencing a variety of cellular processes within joint tissues. Calcium is essential for regulating key cellular functions, including gene expression, muscle contraction, cell cycle progression, proliferation, apoptosis, excitation-contraction coupling, synaptic transmission, and embryonic development. Particularly, in the context of arthritic diseases, an imbalance in calcium homeostasis has significant consequences, since the osteogenic and chondrogenic processes, as well as extracellular matrix formation, are highly influenced by calcium levels. Given these insights, a deeper understanding of the mechanisms governing calcium uptake, release, and metabolism could enhance our comprehension of disease pathogenesis and facilitate the development of novel therapeutic strategies. This review provides an overview of calcium signaling mechanisms, particularly in the most affected cells and tissues in rheumatoid arthritis and osteoarthritis, and summarizes the emerging therapies targeting calcium metabolism that may improve current treatment options.
类风湿关节炎和骨关节炎是世界范围内最普遍的慢性疾病,对患者和卫生保健系统都造成了重大负担。尽管它们的病因和进展不同,但新出现的证据表明,钙信号通过影响关节组织内的多种细胞过程,在这两种疾病的发病机制中起着关键作用。钙对调节关键细胞功能至关重要,包括基因表达、肌肉收缩、细胞周期进展、增殖、凋亡、兴奋-收缩耦合、突触传递和胚胎发育。特别是,在关节炎疾病的情况下,钙稳态失衡会产生严重后果,因为成骨和软骨形成过程以及细胞外基质的形成受到钙水平的高度影响。鉴于这些见解,对钙摄取、释放和代谢机制的更深入了解可以增强我们对疾病发病机制的理解,并促进新的治疗策略的发展。本文综述了钙信号传导机制,特别是在类风湿性关节炎和骨关节炎中最受影响的细胞和组织中,并总结了针对钙代谢的新疗法,这些疗法可能会改善目前的治疗方案。
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引用次数: 0
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Autoimmunity reviews
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