Inflammation and Cardiovascular Disease: From Pathogenesis to Therapeutic Target

Abstract

Atherosclerosis represents the most common pathological substrate of coronary heart disease (CHD), and the characterization of the disease as a chronic low-grade inflammatory condition is now largely accepted. A number of mediators of inflammation have been widely studied, both as surrogate biomarkers and as causal agents, in the pathophysiological network of atherogenesis and plaque vulnerability. The epidemiological observation that biomarkers of inflammation are associated with clinical cardiovascular risk supports the theory that targeted anti-inflammatory treatment appears to be a promising strategy in reducing residual cardiovascular risk on the background of traditional medical therapy. A large number of randomized controlled trials have shown that drugs commonly used in cardiovascular disease (CVD), such as statins, may be effective in the primary and secondary prevention of cardiovascular events through an anti-inflammatory effect. Moreover, several anti-inflammatory drugs are being tested for their potential to reduce residual cardiovascular risk on the background of validated medical therapy for atherosclerotic disease. In this paper, we review relevant evidence with regard to the relationship between inflammation and CVD, from pathogenesis to therapeutic strategies.

Interleukin-10 overexpression improves the function of endothelial progenitor cells stimulated with TNF-α through the activation of the STAT3 signaling pathway

“…In the past decades, the potential pathogenesis of inflammation in cardiovascular disease (17), lung cancer (18), pulmonary hypertension (19), vascular injury (20) and diabetes (21) has been extensively investigated. Thus, anti-inflammation mediators play a critical role in treatment for diseases.…”

Pathogenesis of Takotsubo Syndrome

“…50 However, in the recent published TROTA study (ThROmbophylia in TAkotsubo cardiomyopathy) 51 Cecchi et al documented that prevalence of thrombophilic disorders in patients with TTS was similar to controls, therefore the role of trombophilic disorder as predisposing factor of this syndrome seems unlikely. 52 …”

Giant Cell Arteritis: Beyond Corticosteroids

“…The use of non-immunological therapy needs to be further elucidated, building on the equivocal evidence for aspirin. In particular, statins (HMG-CoA reductase inhibitors) and renin-angiotensin antagonists are thought to be effective in atherosclerotic disease, partly through antiinflammatory actions [69,70]. Interestingly, angiotensin receptor antagonists have been associated with a lower relapse rate and a corticosteroid-sparing effect in a cohort study of 106 patients [71].…”