Inflammatory Cytokines and Atherosclerotic Plaque Progression. Therapeutic Implications

Abstract

Purpose of the Review Inflammatory cytokines play a major role in atherosclerotic plaque progression. This review summarizes the rationale for personalized anti-inflammatory therapy. Recent Findings Systemic inflammatory parameters may be used to follow the clinical outcome in primary and secondary prevention. Medical therapy, both in patients with stable cardiovascular disease, or with acute events, may be tailored taking into consideration the level and course of systemic inflammatory mediators. There is significant space for improvement in primary prevention and in the treatment of patients who have suffered from severe cardiovascular events, paying attention to not only blood pressure and cholesterol levels but also including inflammatory parameters in our clinical analysis. Summary The potential exists to alter the course of atherosclerosis with anti-inflammatory drugs. With increased understanding of the specific mechanisms that regulate the relationship between inflammation and atherosclerosis, new, more effective and specific anti-inflammatory treatment may become available.

Biomarkers Identification and Therapy Target in Macrophage of Atherosclerosis: Systematic Review

“…Support data from preclinical research [65] that generated mice lacking both apoE and IL-1β The other study in vivo [66], XMA052 MG1K, a chimeric murine version of XOMA 052, inhibited the formation of atherosclerotic lesions in the ApoE−/− model at all three doses tested. This effect was comparable to that reported for complete genetic ablation of IL-1β or IL-1R1 on an ApoE−/− background and was associated with decreases in plasma non-HDL/HDL cholesterol ratio and plaque lipid content and macrophage infiltration, demonstrate for the 1 st time that an antibody targeting IL-1β can inhibit the progression of atherosclerosis in vivo, highlighting the importance of this key cytokine in cardiovascular disease [67][68][69][70][71][72][73][74][75][76][77][78].…”

Hyaluronic Acid-Functionalized Mesoporous Silica Nanoparticles Loading Simvastatin for Targeted Therapy of Atherosclerosis

“…Proinflammatory cytokines are detrimental factors in the pathogenesis of atherosclerosis [46]. Therefore, typical pro-inflammatory cytokines, namely TNF-α and IL-6 secreted by RAW264.7 cells after different treatments, were quantified by ELISA.…”

The correlation of lncRNA SNHG16 with inflammatory cytokines, adhesion molecules, disease severity, and prognosis in acute ischemic stroke patients

“…11,18,19 (b) Less vascular inflammation was related to a lower risk of rupture of the atherosclerotic plaque in the cranial blood vessels and further led to a preserved neurological function and milder disease severity (reflected by the NIHSS score) in AIS patients. [20][21][22] (c) LncRNA SNHG16 was negatively related to adhesion molecules as discussed earlier, which might further inhibit the migration and proliferation of VSMCs, thereby suppressing the formation of foam cell in subendothelial space and preventing the progression of atherosclerosis, thus leading to lower disease severity in AIS patients. 23 In order to determine the prognostic value of lncRNA SNHG16 in AIS management, the recurrence and mortality events were recorded during the follow-up period, then RFS and OS were analyzed by K-M curve and log-rank tests.…”