Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism

<i>Introduction</i>: Psoriatic arthritis (PsA) is a chronic inflammatory disease associated with heightened cardiovascular morbidity, primarily due to accelerated atherosclerosis. Despite increasing evidence linking PsA to endothelial dysfunction, dyslipidemia, and chronic inflammation, cardiovascular risk assessment in PsA remains underdeveloped. This literature review synthesizes current evidence on the shared pathophysiological mechanisms between PsA and atherosclerosis. <i>Materials and methods</i>: A systematic search of PubMed, MEDLINE, Embase, Cochrane Library, Web of Science, and Scopus was conducted to identify studies published between 1990 and 2025. Studies were selected based on relevance to inflammatory pathways, lipid metabolism, and immune-mediated endothelial dysfunction in PsA-related atherosclerosis. <i>Results</i>: PsA contributes to atherosclerosis through persistent systemic inflammation, driven by key cytokines such as IL-17, IL-23, TNF-α, and IL-22. These mediators promote endothelial dysfunction, increased leukocyte adhesion, and plaque formation. Altered lipid metabolism in PsA patients, particularly dysfunctional HDL characterized by impaired cholesterol efflux and pro-inflammatory modifications, further exacerbates cardiovascular risk. Additionally, a disrupted Th17/Treg balance perpetuates vascular inflammation and atherogenesis. The interplay between immune dysregulation and metabolic alterations underscores the systemic nature of PsA and its cardiovascular complications. <i>Conclusion</i>: PsA-associated systemic inflammation accelerates atherosclerosis through immune-mediated endothelial dysfunction and lipid metabolism disturbances. Current cardiovascular risk assessment models fail to capture this increased burden. Targeting IL-17, IL-23, and TNF-α, alongside restoring HDL functionality, may offer novel therapeutic strategies. Future research should focus on longitudinal studies to better characterize cardiovascular outcomes in PsA patients and guide tailored interventions to mitigate atherosclerotic risk.

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Publication Details

Journal
American Journal of BioScience
Published
2025-04-17
DOI
https://doi.org/10.11648/j.ajbio.20251302.13
Primary Topic
Psoriasis: Treatment and Pathogenesis
Type
article
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article

Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism

Eugeniu Russu, Marius Semionov
American Journal of BioScience
Psoriasis: Treatment and Pathogenesis
article

Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism

Eugeniu Russu, Marius Semionov
article en

Abstract

<i>Introduction</i>: Psoriatic arthritis (PsA) is a chronic inflammatory disease associated with heightened cardiovascular morbidity, primarily due to accelerated atherosclerosis. Despite increasing evidence linking PsA to endothelial dysfunction, dyslipidemia, and chronic inflammation, cardiovascular risk assessment in PsA remains underdeveloped. This literature review synthesizes current evidence on the shared pathophysiological mechanisms between PsA and atherosclerosis. <i>Materials and methods</i>: A systematic search of PubMed, MEDLINE, Embase, Cochrane Library, Web of Science, and Scopus was conducted to identify studies published between 1990 and 2025. Studies were selected based on relevance to inflammatory pathways, lipid metabolism, and immune-mediated endothelial dysfunction in PsA-related atherosclerosis. <i>Results</i>: PsA contributes to atherosclerosis through persistent systemic inflammation, driven by key cytokines such as IL-17, IL-23, TNF-α, and IL-22. These mediators promote endothelial dysfunction, increased leukocyte adhesion, and plaque formation. Altered lipid metabolism in PsA patients, particularly dysfunctional HDL characterized by impaired cholesterol efflux and pro-inflammatory modifications, further exacerbates cardiovascular risk. Additionally, a disrupted Th17/Treg balance perpetuates vascular inflammation and atherogenesis. The interplay between immune dysregulation and metabolic alterations underscores the systemic nature of PsA and its cardiovascular complications. <i>Conclusion</i>: PsA-associated systemic inflammation accelerates atherosclerosis through immune-mediated endothelial dysfunction and lipid metabolism disturbances. Current cardiovascular risk assessment models fail to capture this increased burden. Targeting IL-17, IL-23, and TNF-α, alongside restoring HDL functionality, may offer novel therapeutic strategies. Future research should focus on longitudinal studies to better characterize cardiovascular outcomes in PsA patients and guide tailored interventions to mitigate atherosclerotic risk.

American Journal of BioScienceVol. 13(2)
Nicolae Testemițanu State University of Medicine and Pharmacy (MD)
Openalex Percentile: Top 89%
Psoriasis: Treatment and Pathogenesis
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