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International Journal of Rheumatic Diseases最新文献

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Flagellate Erythema: An Indicator of Underlying Malignancy in Dermatomyositis 鞭毛状红斑:皮肌炎潜在恶性肿瘤的一个指标。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-27 DOI: 10.1111/1756-185x.70534
Hieu Chi Ha, On Bon Louis Chan, Anousha Yazdabadi, Christopher Meng Kit Fong
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引用次数: 0
Deforming Arthritis as a New Rheumatologic Manifestation of Cocaine Use 变形性关节炎是可卡因使用的一种新的风湿病表现。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-26 DOI: 10.1111/1756-185x.70529
Michael A. Vierra, Amr Edrees
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引用次数: 0
The Multifaceted Role of p53 in Musculoskeletal Diseases: A Comprehensive Review p53在肌肉骨骼疾病中的多重作用:综述
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-26 DOI: 10.1111/1756-185x.70523
Marofe Hossain, Sun Hao, Ahamed Yeasin, Yongxiang Wang

Background

While extensively studied for its central role in tumor suppression (regulating cell cycle, DNA repair, and apoptosis), the p53 gene is now recognized for its significant involvement in musculoskeletal diseases. Aberrant p53 expression and function are key factors in the pathogenesis and progression, although the specific mechanisms and clinical change potential remain incompletely defined.

Objective

This review systematically summarizes the multifaceted roles of p53 in major musculoskeletal diseases, analyzes the molecular mechanisms driving disease progression, and evaluates its potential as a therapeutic target.

Methods

A comprehensive literature search was conducted in PubMed January 2008 to March 2025 using keywords including P53, osteoporosis, osteoarthritis, rheumatoid arthritis, gout, low back pain, and scoliosis. Original research, reviews, and clinical trials focusing on p53 mechanisms were included. 90 relevant articles were selected for analysis.

Results & Conclusion

p53 critically influences the development and progression of musculoskeletal diseases (osteoporosis, osteoarthritis, rheumatoid arthritis, low back pain, gout, and scoliosis) through diverse mechanisms: Disrupting bone formation/resorption balance (via the p53-Nedd4-Runx2 axis in osteoporosis). Promoting chondrocyte apoptosis (via the miR-34a-SIRT1-p53 pathway in osteoarthritis). Modulating inflammatory mediators (TNF-α, IL-6 in rheumatoid arthritis). Regulating oxidative stress responses (p53-SLC2A9 axis in gout). p53 exhibits dual roles (pro-apoptotic vs. anti-inflammatory), necessitating precise targeting strategies. Promising therapeutic interventions include p53-focused gene editing (CRISPR/Cas9), small-molecule inhibitors (PFT-α), and natural products (naringin). However, further clinical validation is essential. Future research requires multidisciplinary approaches to deepen understanding of p53 mechanisms and advance clinical applications in musculoskeletal disorders.

背景:虽然p53基因在肿瘤抑制(调节细胞周期、DNA修复和细胞凋亡)中的核心作用被广泛研究,但现在人们认识到它在肌肉骨骼疾病中的重要作用。p53的异常表达和功能是其发病和进展的关键因素,但其具体机制和临床变化潜力尚未完全确定。目的:本文系统总结了p53在主要肌肉骨骼疾病中的多方面作用,分析了其驱动疾病进展的分子机制,并评估了其作为治疗靶点的潜力。方法:在PubMed 2008年1月至2025年3月检索相关文献,检索关键词为P53、骨质疏松症、骨关节炎、类风湿关节炎、痛风、腰痛、脊柱侧凸。原始研究,综述和临床试验集中在p53机制包括。选取90篇相关文章进行分析。结果与结论:p53通过多种机制严重影响肌肉骨骼疾病(骨质疏松症、骨关节炎、类风湿性关节炎、腰痛、痛风和脊柱侧弯)的发生和进展:破坏骨形成/吸收平衡(在骨质疏松症中通过p53- nedd4 - runx2轴)。促进软骨细胞凋亡(通过miR-34a-SIRT1-p53通路在骨关节炎中)。类风湿关节炎中调节炎症介质(TNF-α, IL-6)。调节痛风中的氧化应激反应(p53-SLC2A9轴)。P53表现出双重作用(促凋亡和抗炎),需要精确的靶向策略。有希望的治疗干预措施包括p53靶向基因编辑(CRISPR/Cas9)、小分子抑制剂(PFT-α)和天然产物(柚皮苷)。然而,进一步的临床验证是必要的。未来的研究需要多学科的方法来加深对p53机制的理解,并推进在肌肉骨骼疾病中的临床应用。
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引用次数: 0
Systemic Lupus Erythematosus and Multiple Sclerosis Overlap After Adalimumab Therapy: A Case Report 阿达木单抗治疗后系统性红斑狼疮和多发性硬化症重叠:一例报告。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-25 DOI: 10.1111/1756-185x.70527
María García-González, Andrea Fernández-Valmaña, Jesús Alberto López-Martínez, Marta Ros-Segura, Carlos Feijoo-Massó
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引用次数: 0
Potential Significance of CCL17 in Psoriatic Arthritis CCL17在银屑病关节炎中的潜在意义。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-23 DOI: 10.1111/1756-185x.70526
Kevin Ming-Chin Lee, Adrian A. Achuthan, Matthew Jiang, John A. Hamilton, Keith Lim
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引用次数: 0
Epidemiology of Rheumatic and Musculoskeletal Disorders in Province 3 of Nepal: A COPCORD-Based Community Survey 尼泊尔第3省风湿病和肌肉骨骼疾病的流行病学:基于copcord的社区调查
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-21 DOI: 10.1111/1756-185x.70507
Binit Vaidya, Shweta Nakarmi
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引用次数: 0
Tocilizumab in the Treatment of Sporadic Inclusion Body Myositis 托珠单抗治疗散发性包涵体肌炎。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-21 DOI: 10.1111/1756-185x.70521
Cheng Xu, Ning Shen, Yongmei Han
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引用次数: 0
Risk of Pneumocystis Pneumonia in Patients With Rheumatoid Arthritis and the Role of Prophylactic Salazosulfapyridine 类风湿关节炎患者肺囊虫性肺炎的风险及预防性磺胺吡啶的作用。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-21 DOI: 10.1111/1756-185x.70516
Ryo Sato, Kenya Terabe, Takahiro Imaizumi, Koji Sakamoto, Kikue Sato, Junya Hasegawa, Takaya Sugiura, Yusuke Ono, Mochihito Suzuki, Shuji Asai, Shiro Imagama

Objectives

This study aimed to assess the risk factors for Pneumocystis pneumonia (PCP) in patients with rheumatoid arthritis (RA) and investigate the potential of salazosulfapyridine (SASP) as a prophylactic agent.

Methods

The present study analyzed data from the Japanese Diagnosis Procedure Combination database, which provides comprehensive inpatient data (including diagnoses, procedures, and medications) covering a large portion of the population. We identified patients with RA who developed PCP among 14 190 patients diagnosed with RA at admission with a treatment history. Patients with RA who were receiving therapeutic doses of drugs for PCP were defined as having PCP. A nested case–control analysis was performed to compare patients with RA and PCP with age- and sex-matched control patients with RA without PCP in a ratio of 1:20.

Results

The cohort comprised 132 patients with PCP and 2575 controls. The risk factors for PCP in RA were chronic obstructive pulmonary disease, methotrexate (MTX), biological/targeted synthetic DMARDs (b/tsDMARDs), and high-dose glucocorticoids. SASP may have a protective effect against PCP, particularly in patients with RA treated with MTX and/or b/tsDMARDs.

Conclusion

The large sample size of the present study suggests that SASP may be associated with a reduced PCP risk in RA patients.

目的:本研究旨在评估类风湿关节炎(RA)患者肺囊虫性肺炎(PCP)的危险因素,并探讨salazosulfapyridine (SASP)作为预防药物的潜力。方法:本研究分析了来自日本诊断程序组合数据库的数据,该数据库提供了涵盖大部分人口的全面住院数据(包括诊断,程序和药物)。我们在14190名入院时有治疗史的RA患者中发现了出现PCP的RA患者。接受PCP治疗剂量的RA患者被定义为PCP患者。进行巢式病例对照分析,将RA和PCP患者与年龄和性别匹配的RA无PCP对照患者以1:20的比例进行比较。结果:该队列包括132例PCP患者和2575例对照。慢性阻塞性肺疾病、甲氨蝶呤(MTX)、生物/靶向合成DMARDs (b/tsDMARDs)和大剂量糖皮质激素是RA中PCP的危险因素。SASP可能对PCP有保护作用,特别是在接受MTX和/或b/tsDMARDs治疗的RA患者中。结论:本研究的大样本量表明SASP可能与RA患者PCP风险降低有关。
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引用次数: 0
Variable Expression of CD62L (L-Selectin) on Various White Blood Cells in Rheumatoid Arthritis CD62L (l -选择素)在类风湿关节炎不同白细胞中的表达变化
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-21 DOI: 10.1111/1756-185x.70519
Bidyalaxmi Leishangthem, Aastha Khullar, Chandra Bhushan Prasad, Sankar Jayaprakash, Siddharth Jain, Varun Dhir
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引用次数: 0
Dual Mechanisms of Hyperuricemia-Associated Renal Injury: A Systematic Review of Crystal-Dependent and Crystal-Independent Pathways 高尿酸血症相关肾损伤的双重机制:晶体依赖性和晶体非依赖性途径的系统综述。
IF 2 4区 医学 Q2 RHEUMATOLOGY Pub Date : 2025-12-21 DOI: 10.1111/1756-185x.70493
Gudisa Bereda, Felix Pius Omullo

Background

Hyperuricemia, marked by elevated uric acid levels, is associated with renal disorders like acute kidney injury and chronic kidney disease, through both crystal-dependent and crystal-independent mechanisms.

Objective

This review aims to evaluate the crystal-dependent and crystal-independent mechanisms by which hyperuricemia induces renal injury.

Design

A systematic review of the literature.

Participants

Human and animal studies.

Measurements

A total of 1549 articles were initially identified from PubMed, Web of Science, Scopus, and Google Scholar. After removing 659 duplicates and screening titles and abstracts, 572 articles were excluded, and 16 could not be retrieved, leaving 302 for full-text review. Of these, 17 studies met the eligibility criteria and were included. Risk of bias was assessed using SYRCLE for animal studies, ROB2 for human studies, and NOS for observational studies.

Results

From 17 studies: nine animal experiments, one human experiment, and seven observational studies. Animal studies showed hyperuricemia causes preglomerular arteriolopathy, glomerular hypertension, and worsens nephrotoxicity. Human studies demonstrated elevated uric acid, even without crystals, activates intrarenal RAS, increases oxidative stress, and reduces nitric oxide. Clinical studies confirmed high uric acid is linked to CKD progression, with very low levels also risky (“J-shaped” relationship). Endothelial dysfunction is a unifying mechanism, promoting inflammation and fibrosis in crystal-dependent injury and vasoconstriction and renal damage in crystal-independent injury.

Conclusions

This review confirmed that hyperuricemia damages the kidney through both crystal-dependent and crystal-independent pathways, with endothelial dysfunction as a key mediator. Further human studies are needed to confirm these findings and explore new treatments.

背景:以尿酸水平升高为标志的高尿酸血症,通过晶体依赖性和晶体非依赖性机制与急性肾损伤和慢性肾脏疾病等肾脏疾病相关。目的:探讨高尿酸血症引起肾损伤的晶体依赖性和晶体非依赖性机制。设计:对文献进行系统回顾。参与者:人类和动物研究。测量:最初从PubMed、Web of Science、Scopus和谷歌Scholar中共鉴定出1549篇文章。在删除659篇重复文章并筛选标题和摘要后,572篇文章被排除,16篇无法检索,剩下302篇进行全文审查。其中,17项研究符合入选标准。动物研究采用sycle评估偏倚风险,人类研究采用ROB2评估,观察性研究采用NOS评估。结果:17项研究:9项动物实验,1项人体实验,7项观察性研究。动物研究表明,高尿酸血症可引起肾小球前动脉病变、肾小球高血压,并加重肾毒性。人体研究表明,尿酸升高,即使没有结晶,也会激活肾内RAS,增加氧化应激,减少一氧化氮。临床研究证实,高尿酸与CKD进展有关,非常低的尿酸水平也有风险(“j型”关系)。内皮功能障碍是一个统一的机制,在晶体依赖性损伤中促进炎症和纤维化,在晶体非依赖性损伤中促进血管收缩和肾损害。结论:本综述证实,高尿酸血症通过晶体依赖性和晶体非依赖性途径损害肾脏,内皮功能障碍是一个关键的中介。需要进一步的人体研究来证实这些发现并探索新的治疗方法。
{"title":"Dual Mechanisms of Hyperuricemia-Associated Renal Injury: A Systematic Review of Crystal-Dependent and Crystal-Independent Pathways","authors":"Gudisa Bereda,&nbsp;Felix Pius Omullo","doi":"10.1111/1756-185x.70493","DOIUrl":"10.1111/1756-185x.70493","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hyperuricemia, marked by elevated uric acid levels, is associated with renal disorders like acute kidney injury and chronic kidney disease, through both crystal-dependent and crystal-independent mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This review aims to evaluate the crystal-dependent and crystal-independent mechanisms by which hyperuricemia induces renal injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>A systematic review of the literature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Participants</h3>\u0000 \u0000 <p>Human and animal studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Measurements</h3>\u0000 \u0000 <p>A total of 1549 articles were initially identified from PubMed, Web of Science, Scopus, and Google Scholar. After removing 659 duplicates and screening titles and abstracts, 572 articles were excluded, and 16 could not be retrieved, leaving 302 for full-text review. Of these, 17 studies met the eligibility criteria and were included. Risk of bias was assessed using SYRCLE for animal studies, ROB2 for human studies, and NOS for observational studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From 17 studies: nine animal experiments, one human experiment, and seven observational studies. Animal studies showed hyperuricemia causes preglomerular arteriolopathy, glomerular hypertension, and worsens nephrotoxicity. Human studies demonstrated elevated uric acid, even without crystals, activates intrarenal RAS, increases oxidative stress, and reduces nitric oxide. Clinical studies confirmed high uric acid is linked to CKD progression, with very low levels also risky (“J-shaped” relationship). Endothelial dysfunction is a unifying mechanism, promoting inflammation and fibrosis in crystal-dependent injury and vasoconstriction and renal damage in crystal-independent injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This review confirmed that hyperuricemia damages the kidney through both crystal-dependent and crystal-independent pathways, with endothelial dysfunction as a key mediator. Further human studies are needed to confirm these findings and explore new treatments.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 12","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145803574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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International Journal of Rheumatic Diseases
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