Cardiometabolic Risk in Psoriatic Arthritis: A Hidden Burden of Inflammation and Metabolic Dysregulation.

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Metabolites Pub Date : 2025-03-18 DOI:10.3390/metabo15030206
Mislav Radić, Andrej Belančić, Hana Đogaš, Marijana Vučković, Yusuf Ziya Sener, Seher Sener, Almir Fajkić, Josipa Radić
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Abstract

Psoriatic arthritis (PsA) is a chronic inflammatory disease that extends beyond musculoskeletal and dermatologic involvement to elevate cardiometabolic risk. Emerging evidence highlights the critical role of systemic inflammation in metabolic dysregulation, accelerating insulin resistance, dyslipidemia, and oxidative stress, all of which contribute to the increased burden of cardiovascular disease in PsA. This review explores the intricate interplay between inflammatory mediators-such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17),-adipokine imbalances, and lipid metabolism abnormalities, all of which foster endothelial dysfunction and atherosclerosis. The dysregulation of adipokines, including leptin, adiponectin, and resistin, further perpetuates inflammatory cascades, exacerbating cardiovascular risk. Additionally, the metabolic alterations seen in PsA, particularly insulin resistance and lipid dysfunction, not only contribute to cardiovascular comorbidities but also impact disease severity and therapeutic response. Understanding these mechanistic links is imperative for refining risk stratification strategies and tailoring interventions. By integrating targeted immunomodulatory therapies with metabolic and cardiovascular risk management, a more comprehensive approach to PsA treatment can be achieved. Future research must focus on elucidating shared inflammatory and metabolic pathways, enabling the development of innovative therapeutic strategies to mitigate both systemic inflammation and cardiometabolic complications in PsA.

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银屑病关节炎的心脏代谢风险:炎症和代谢失调的隐藏负担。
银屑病关节炎(PsA)是一种慢性炎症性疾病,超越肌肉骨骼和皮肤的参与,提高心脏代谢的风险。新出现的证据强调了全身性炎症在代谢失调、加速胰岛素抵抗、血脂异常和氧化应激中的关键作用,所有这些都有助于增加PsA中心血管疾病的负担。这篇综述探讨了炎症介质之间复杂的相互作用,如肿瘤坏死因子-α (TNF-α)、白细胞介素-6 (IL-6)和白细胞介素-17 (IL-17)、脂肪因子失衡和脂质代谢异常,所有这些都促进了内皮功能障碍和动脉粥样硬化。脂肪因子(包括瘦素、脂联素和抵抗素)的失调,进一步加剧了炎症级联反应,加剧了心血管风险。此外,PsA的代谢改变,尤其是胰岛素抵抗和脂质功能障碍,不仅会导致心血管合并症,还会影响疾病的严重程度和治疗反应。了解这些机制联系对于完善风险分层策略和调整干预措施至关重要。通过将靶向免疫调节疗法与代谢和心血管风险管理相结合,可以实现更全面的PsA治疗方法。未来的研究必须集中于阐明共同的炎症和代谢途径,从而开发出创新的治疗策略,以减轻PsA的全身炎症和心脏代谢并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Metabolites
Metabolites Biochemistry, Genetics and Molecular Biology-Molecular Biology
CiteScore
5.70
自引率
7.30%
发文量
1070
审稿时长
17.17 days
期刊介绍: Metabolites (ISSN 2218-1989) is an international, peer-reviewed open access journal of metabolism and metabolomics. Metabolites publishes original research articles and review articles in all molecular aspects of metabolism relevant to the fields of metabolomics, metabolic biochemistry, computational and systems biology, biotechnology and medicine, with a particular focus on the biological roles of metabolites and small molecule biomarkers. Metabolites encourages scientists to publish their experimental and theoretical results in as much detail as possible. Therefore, there is no restriction on article length. Sufficient experimental details must be provided to enable the results to be accurately reproduced. Electronic material representing additional figures, materials and methods explanation, or supporting results and evidence can be submitted with the main manuscript as supplementary material.
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