Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target.

We are witnessing the globalization of a specific type of arteriosclerosis with rising prevalence, incidence and an overall cardiovascular disease burden. Currently, atherosclerosis increasingly affects the younger generation as compared to previous decades. While early preventive medicine has seen improvements, research advances in laboratory and clinical investigation promise to provide us with novel diagnosis tools. Given the physio-pathological complexity and epigenetic patterns of atherosclerosis and the discovery of new molecules involved, the therapeutic field of atherosclerosis has room for substantial growth. Thus, the scientific community is currently investigating the role of nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a crucial component of the innate immune system in different inflammatory disorders. NLRP3 is activated by distinct factors and numerous cellular and molecular events which trigger NLRP3 inflammasome assembly with subsequent cleavage of pro-interleukin (IL)-1β and pro-IL-18 pathways via caspase-1 activation, eliciting endothelial dysfunction, promotion of oxidative stress and the inflammation process of atherosclerosis. In this review, we introduce the basic cellular and molecular mechanisms of NLRP3 inflammasome activation and its role in atherosclerosis. We also emphasize its promising therapeutic pharmaceutical potential.

Oral microbiota formation begins from birth, and everything from genetic components to the environment, alongside the host’s behavior (such as diet, smoking, oral hygiene, and even physical activity), contributes to oral microbiota structure. Even though recent studies have focused on the gut microbiota’s role in systemic diseases, the oral microbiome represents the second largest community of microorganisms, making it a new promising therapeutic target. Periodontitis and dental caries are considered the two main consequences of oral bacterial imbalance. Studies have shown that oral dysbiosis effects are not limited locally. Due to technological advancement, research identified oral bacterial species in heart valves. This evidence links oral dysbiosis with the development of valvular heart disease (VHD). This review focuses on describing the mechanism behind prolonged local inflammation and dysbiosis, that can induce bacteriemia by direct or immune-mediated mechanisms and finally VHD. Additionally, we highlight emerging therapies based on controlling oral dysbiosis, periodontal disease, and inflammation with immunological and systemic effects, that exert beneficial effects in VHD management.