Free radicals and endothelial dysfunction: Potential positive effects of TNF-α inhibitors

Abstract

TNF-α inhibitors may change the progression of endothelial dysfunction and, thus, slow down the atherosclerotic process.

Patient reports of the frequency and severity of adverse reactions associated with biological agents prescribed for psoriasis in Brazil

“…TNF-a inhibitors decrease serum levels of inflammatory markers such as TNF-a itself, C-reactive protein, IL-6 and increase the tissue expression of endothelial nitric oxide synthase and the vasodilatory response to bradykinin. TNF-a inhibitors alter the progression of endothelial dysfunction and may decrease the atherosclerotic process [22]. TNF-a inhibitors thus reduce the systemic inflammation in patients with chronic immune-mediated diseases and improve the endothelial function, potentially decreasing the risk of Pulmonary arterial hypertension progression [23].…”

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes

“…Several meta-analyses confirm dysregulated levels of inflammatory cytokines in major depression (76,142,144,202). The role and importance of inflammatory cytokines in inducing aberrant endothelial function was examined in several studies (94,235,255,297). For instance, TNF-␣ and IL-1 decrease eNOS activity along with reducing eNOS mRNA and protein content (379) while at the same time also reducing vasodilatory response to bradykinin and arachidonic acid in human cutaneous vessels.…”

Use of leflunomide plus TNF-α inhibitors in rheumatoid arthritis

“…Etanercept and adalimumab may exert beneficial effects on lipid profile improving the endothelial dysfunction [29]. TNF-a inhibitors improves both the clinical course of RA and the endothelial function and, thus, may decrease the risk of acute cardiovascular and/or cerebrovascular events [25,[30][31][32]. These findings suggest that the therapeutic combination LFN plus one TNF-a inhibitor could play a beneficial role in the treatment of accelerated atherosclerosis in patients with RA or other immune-mediated diseases.…”

“…Therefore, LFN is an anti-atherogenic drug and its administration could decrease the risk of developing [24]. Furthermore, TNF-a inhibitors reduce the expression of vascular endothelial growth factor (VEGF), nitric oxide (NO) and inducible NO synthase [25,26]. VEGF, which is a critical mediator of inflammation both in chronic immune-mediated and allergic diseases, is a pro-angiogenic factor which alters the microvascular network and contributes to the development and progression of atherosclerosis [25,27,28].…”

“…Furthermore, TNF-a inhibitors reduce the expression of vascular endothelial growth factor (VEGF), nitric oxide (NO) and inducible NO synthase [25,26]. VEGF, which is a critical mediator of inflammation both in chronic immune-mediated and allergic diseases, is a pro-angiogenic factor which alters the microvascular network and contributes to the development and progression of atherosclerosis [25,27,28]. Etanercept and adalimumab may exert beneficial effects on lipid profile improving the endothelial dysfunction [29].…”