Journal Article Review Epublish
PubMed: 40137170 DOI: 10.3390/metabo15030206
Cardiometabolic Risk in Psoriatic Arthritis: A Hidden Burden of Inflammation and Metabolic Dysregulation.
Metabolites 15(3)
Authors: Mislav Radić, Andrej Belančić, Hana Đogaš, Marijana Vučković, Yusuf Ziya Sener, Seher Sener, Almir Fajkić, Josipa Radić
Affiliations
- 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.
- Department of Basic and Clinical Pharmacology with Toxicology, Faculty of Medicine, University of Rijeka, Braće Branchetta 20, 51000 Rijeka, Croatia.
- Department of Neurology, University Hospital of Split, 21000 Split, Croatia.
- Department of Internal Medicine, Division of Nephrology and Dialysis, University Hospital of Split, 21000 Split, Croatia.
- Department of Pediatric Rheumatology, Sophia Children's Hospital, Erasmus University Medical Center, 3000 CB Rotterdam, The Netherlands.
- Department of Cardiology, Thoraxcenter, Erasmus University Medical Center, 3000 CB Rotterdam, The Netherlands.
- Department of Pathophysiology, Faculty of Medicine, University of Sarajevo, 71000 Sarajevo, Bosnia and Herzegovina.
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.
MeSH
Arthritis, Psoriatic, Insulin Resistance, Tumor Necrosis Factor-Alpha, Insulin, Dyslipidemias, Arthritis, Interleukin-6, Risk Management, Oxidative Stress, Therapeutics, Adipokines, Interleukin-17