Atherosclerosis and inflammation: overview and updates

Abstract

The concept that inflammation participates pivotally in the pathogenesis of atherosclerosis and its complications has gained considerable attention, but has not yet entered clinical practice. Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. The recognition of atherogenesis as an active process rather than a cholesterol storage disease or a repository of calcium has highlighted some key inflammatory mechanisms. For example, mononuclear phagocytes contribute to all stages of this disease, illustrating the link between inflammation and atherosclerosis. From a clinical perspective, harnessing inflammation may now help target therapeutics, change guidelines, and enter daily practice. Multiple lines of incontrovertible evidence have proven a causal role for low-density lipoprotein (LDL) cholesterol in atherosclerosis, and we have highly effective tools for lowering LDL, consequently reducing events. Yet, even with intense LDL reduction, events still occur. Inflammation can explain some of this residual risk. An anti-inflammatory intervention has now proven capable of improving outcomes in individuals well treated with LDL-lowering agents. A suite of trials are now pursuing anti-inflammatory therapies in this context. Assessment and treatment of residual inflammatory risk are poised to provide new inroads into preventive cardiology. This brief review aims to explore the potential mechanisms underlying the association of inflammation and atherogenesis, and their clinical consequences.

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

“…Inflammation is considered a main process involved in atherosclerosis development [74]. A recent meta-analysis of nine RCTs and 509 patients showed that the CoQ 10 supplementation in chronic inflammatory diseases (60-500 mg/day for 8-12 weeks) is responsible for the significant reduction in the plasma levels of tumor necrosis factor alpha (TNF-α) (SMD: −0.44, 95% CI: (−0.81 to −0.07) mg/dl; I 2 = 66.1%, p < 0.01) and in IL-6 levels (SMD: −0.37, 95% CI: (−0.65 to −0.09), p = 0.01) [75].…”

Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

“…Therefore, we conducted this study and found that both before and after adjustment by age/gender, lncRNA THRIL was greatly enhanced in CHD patients compared to controls, and it showed good predictive value for increased CHD risk. These data could be explained by that: (a) LncRNA THRIL might regulate several pathways (such as TNF‐α and NF‐κB) to induce inflammation as in systemic lupus erythematosus model and osteoarthritis model, which accelerated the process of atherosclerosis and rose the possibility of CHD incidence; (b) it is proposed that lncRNA THRIL activated TNF‐α transcription, and TNF‐α is a major cause of local and systemic insulin resistance . Thus, it was possible that lncRNA THRIL might up‐regulate TNF‐α to increase the risk of diabetes mellitus, one of the risk factors of CHD, thereby enhanced the incidence of CHD.…”

Associations among Bone Mineral Density, Physical Activity and Nutritional Intake in Middle-Aged Women with High Levels of Arterial Stiffness: A Pilot Study

“…Saturated fatty acids, levels of which were significantly elevated in the PWV-High group, have been suggested to be atherogenic through induction of endothelial dysfunction [58,59]. Numerous reports have indicated increased oxidative stress and chronic inflammation in patients with atherosclerosis [60][61][62][63]. Inflammatory cytokines (TNF, IL-6, IL-1), which contribute to inflammatory responses, have been reported to promote osteoclast differentiation [64][65][66][67], and oxidative stress was shown to inhibit osteogenic bone formation and differentiation maturation [21].…”