Radić Mislav, Belančić Andrej, Đogaš Hana, Vučković Marijana, Sener Yusuf Ziya, Sener Seher, Fajkić Almir, Radić Josipa
Department of Internal Medicine, Division of Rheumatology, Allergology and Clinical Immunology, Center of Excellence for Systemic Sclerosis in Croatia, University Hospital of Split, 21000 Split, Croatia.
Internal Medicine Department, School of Medicine, University of Split, 21000 Split, Croatia.
Metabolites. 2025 Mar 18;15(3):206. doi: 10.3390/metabo15030206.
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.
银屑病关节炎（PsA）是一种慢性炎症性疾病，其影响范围不仅限于肌肉骨骼和皮肤，还会增加心脏代谢风险。新出现的证据凸显了全身炎症在代谢失调、加速胰岛素抵抗、血脂异常和氧化应激中的关键作用，所有这些都导致了PsA患者心血管疾病负担的增加。本综述探讨了炎症介质（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之间的复杂相互作用，所有这些都会促进内皮功能障碍和动脉粥样硬化。包括瘦素、脂联素和抵抗素在内的脂肪因子失调会进一步使炎症级联反应持续存在，加剧心血管风险。此外，PsA中出现的代谢改变，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制定个性化干预措施至关重要。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。未来的研究必须专注于阐明共同的炎症和代谢途径，从而开发创新的治疗策略，以减轻PsA中的全身炎症和心脏代谢并发症。
