Introduction: 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. Materials and methods: 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. Results: 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. Conclusion: 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.
| Published in | American Journal of BioScience (Volume 13, Issue 2) |
| DOI | 10.11648/j.ajbio.20251302.13 |
| Page(s) | 55-68 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2025. Published by Science Publishing Group |
Psoriatic Arthritis, Atherosclerosis, Cardiovascular Risk, Endothelial Dysfunction
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APA Style
Semionov, M., Russu, E. (2025). Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism. American Journal of BioScience, 13(2), 55-68. https://doi.org/10.11648/j.ajbio.20251302.13
ACS Style
Semionov, M.; Russu, E. Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism. Am. J. BioScience 2025, 13(2), 55-68. doi: 10.11648/j.ajbio.20251302.13
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Download@article{10.11648/j.ajbio.20251302.13,
author = {Marius Semionov and Eugeniu Russu},
title = {Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism
},
journal = {American Journal of BioScience},
volume = {13},
number = {2},
pages = {55-68},
doi = {10.11648/j.ajbio.20251302.13},
url = {https://doi.org/10.11648/j.ajbio.20251302.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbio.20251302.13},
abstract = {Introduction: 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. Materials and methods: 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. Results: 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. Conclusion: 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.
},
year = {2025}
}
TY - JOUR T1 - Pathophysiology of Atherosclerosis in Psoriatic Arthritis: New Insights into Inflammation and Lipid Metabolism AU - Marius Semionov AU - Eugeniu Russu Y1 - 2025/04/17 PY - 2025 N1 - https://doi.org/10.11648/j.ajbio.20251302.13 DO - 10.11648/j.ajbio.20251302.13 T2 - American Journal of BioScience JF - American Journal of BioScience JO - American Journal of BioScience SP - 55 EP - 68 PB - Science Publishing Group SN - 2330-0167 UR - https://doi.org/10.11648/j.ajbio.20251302.13 AB - Introduction: 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. Materials and methods: 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. Results: 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. Conclusion: 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. VL - 13 IS - 2 ER -
Department of Internal Medicine, Discipline of Rheumatology and Nephrology, State University of Medicine and Pharmacy “Nicolae Testemitanu”, Chisinau, Republic of Moldova
Department of Internal Medicine, Discipline of Rheumatology and Nephrology, State University of Medicine and Pharmacy “Nicolae Testemitanu”, Chisinau, Republic of Moldova; Department of Arthrology, Republican Clinical Hospital “Timofei Mosneaga”, Chisinau, Republic of Moldova
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