Cardiovascular diseases (CVDs) are the prevalent cause of mortality around the world. Activation of inflammasome contributes to the pathological progression of cardiovascular diseases, including atherosclerosis, abdominal aortic aneurysm, myocardial infarction, dilated cardiomyopathy, diabetic cardiomyopathy, heart failure, and calcific aortic valve disease. The nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome plays a critical role in the innate immune response, requiring priming and activation signals to provoke the inflammation. Evidence shows that NLRP3 inflammasome not only boosts the cleavage and release of IL-1 family cytokines, but also leads to a distinct cell programmed death: pyroptosis. The significance of NLRP3 inflammasome in the CVDs-related inflammation has been extensively explored. In this review, we summarized current understandings of the function of NLRP3 inflammasome in CVDs and discussed possible therapeutic options targeting the NLRP3 inflammasome.

Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.

Abdominal aortic aneurysm (AAA) is the most common true aneurysm worldwide, and recent studies suggest that dendritic cells (DCs) play a key role in its development, though the specific subtypes and underlying mechanisms remain unclear. In this study, the role of interferon regulatory factor 8 (IRF8) in AAA is investigated by focusing on its effect on the differentiation of DC precursors into conventional type 1 dendritic cells (cDC1s). It is found significant infiltration of HLA‐DR ⁺ IRF8 ⁺ cells in human AAA tissue samples. In mice, DC‐specific overexpression of Irf8 exacerbates aneurysm expansion following periadventitial elastase application, while DC‐specific Irf8 deletion attenuates AAA development. Batf3 ^−/− mice, which lack cDC1s, exhibit AAA characteristics similar to the Irf8 ‐deleted mice. Additionally, an increased population of activated CD8 ⁺ T cells is observed in the DC‐ Irf8 overexpressed mice, while the DC‐ Irf8 deletion mice show a decrease in these cells. Blocking antigen cross‐presentation to CD8 ⁺ T cells also reduces AAA progression. Tissue microarray analysis of human aortic samples further confirms a correlation between IRF8 expression and AAA development. These findings suggest that IRF8 activation promotes cDC1 differentiation, leading to the recruitment of CD8 ⁺ T cells, which contribute to aortic wall destruction and AAA formation.

Calcific aortic valve disease (CAVD) is a prevalent condition characterized by pathological thickening and calcification of the aortic valve, leading to increased pressure overload and cardiac remodeling, particularly in individuals aged 65 and older. This review synthesizes recent advances in understanding the pathogenesis of CAVD, focusing on key mechanisms including hemodynamic alterations, endothelial dysfunction, lipid deposition, inflammation, and fibrotic calcification. We evaluate emerging therapeutic targets based on pivotal basic research and clinical trials, highlighting the potential for mechanism-oriented interventions. Furthermore, we explore the implications of lipid-lowering therapies, anti-inflammatory strategies, and antifibrocalcific agents, as well as novel bioprosthetic designs aimed at enhancing patient outcomes. Additionally, we discuss the inherent genetic and molecular backgrounds influencing individual susceptibility to CAVD, emphasizing the promise of personalized therapy. By bridging the gap between basic science and clinical application, this review aims to guide future research efforts toward more effective prevention and treatment strategies for CAVD.

Heart transplantation is currently the most effective treatment for end-stage heart failure; however, the shortage in donor hearts constrains the undertaking of transplantation. Mechanical circulatory support (MCS) technology has made rapid progress in recent years, providing diverse therapeutic options and alleviating the dilemma of donor heart shortage. The ventricular assist device (VAD), as an important category of MCS, demonstrates promising applications in bridging heart transplantation, destination therapy, and bridge-to-decision. VADs can be categorized as durable VADs (dVADs) and temporary VADs (tVADs), according to the duration of assistance. With the technological advancement and clinical application experience accumulated, VADs have been developed in biocompatible, lightweight, bionic, and intelligent ways. In this review, we summarize the development history of VADs, focusing on the mechanism and application status of dVADs in detail, and further discuss the research progress and use of VADs in China.