2021
DOI: 10.55563/clinexprheumatol/3qiqk3
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Subclinical atherosclerosis evolution during 5 years of anti-TNF-alpha treatment in psoriatic arthritis patients

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Cited by 13 publications
(4 citation statements)
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“…Thus, changes in cell shape leading to reorganization of actin cytoskeleton can regulate growth and proliferation, making cytoskeleton regulation a potential intervention for atherosclerosis 31 . TNF, one of the proinflammatory cytokines, play an important role in the pathophysiology of the inflammatory arthritis including gout and are associated with the induction and maintenance of the atherosclerosis 32 , 33 .Two studies reported that TNF antagonists may have a beneficial effect on preventing the progression of subclinical atherosclerosis 33 , 34 . Wei Gao et al discovered the underlying mechanism and found that exosomes derived from mature dendritic cells increase atherosclerosis via membrane TNF mediated NF-kB pathway 35 .…”
Section: Discussionmentioning
confidence: 99%
“…Thus, changes in cell shape leading to reorganization of actin cytoskeleton can regulate growth and proliferation, making cytoskeleton regulation a potential intervention for atherosclerosis 31 . TNF, one of the proinflammatory cytokines, play an important role in the pathophysiology of the inflammatory arthritis including gout and are associated with the induction and maintenance of the atherosclerosis 32 , 33 .Two studies reported that TNF antagonists may have a beneficial effect on preventing the progression of subclinical atherosclerosis 33 , 34 . Wei Gao et al discovered the underlying mechanism and found that exosomes derived from mature dendritic cells increase atherosclerosis via membrane TNF mediated NF-kB pathway 35 .…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, human studies have demonstrated that both coronary artery and circulating IL-32 levels were elevated in CAD patients, suggesting that IL-32 was independently related to the existence of CAD and could have played a role in atherosclerotic CAD through modulating the inflammatory response [39]. A recent study on evaluating subclinical atherosclerosis progression after 5 years of anti-TNF-α treatment in psoriatic arthritis patients showed a slight progression of subclinical atherosclerosis in the first 2 years of anti-TNF-α treatment [40]. A study by Puz et al [41] corroborated that TNF-α and IL-6 were involved in atherosclerosis development in patients with internal carotid artery stenosis.…”
Section: Discussionmentioning
confidence: 99%
“…It is possible that CRP and IL-6 are related to CVD outcomes but less related to subclinical disease 35 or resilient to dietary challenges 36 . Pro-inflammatory cytokines, such as TNFα, are widely known to be atherogenic 21 , but studies on the efficacy of TNFα inhibitors to stall progression of SA in high-risk patients has been controversial 37 , 38 . Some studies also reported an association between presence of atherosclerotic plaque with TNFα receptors, but absence of association with TNFα itself 35 .…”
Section: Discussionmentioning
confidence: 99%