Atherosclerosis (AS), a chronic sterile inflammatory disorder, is one of the leading causes of mortality worldwide. The dysfunction and unnatural death of plaque cells, including vascular endothelial cells (VEC), macrophages, and vascular smooth muscle cells (VSMC), are crucial factors in the progression of AS. Pyroptosis was described as a form of cell death at least two decades ago. It is featured by plasma membrane swelling and rupture, cell lysis, and consequent robust release of cytosolic contents and pro-inflammatory mediators, including interleukin-1β (IL-1β), IL-18, and high mobility group box 1 (HMGB1). Pyroptosis of plaque cells is commonly observed in the initiation and development of AS, and the levels of pyroptosis-related proteins are positively correlated with plaque instability, indicating the crucial contribution of pyroptosis to atherogenesis. Furthermore, studies have also identified some candidate anti-atherogenic agents targeting plaque cell pyroptosis. Herein, we summarize the research progress in understating (1) the discovery and definition of pyroptosis; (2) the characterization and molecular mechanisms of pyroptosis; (3) the regulatory mechanisms of pyroptosis in VEC, macrophage, and VSMC, as well as their potential role in AS progression, aimed at providing therapeutic targets for the prevention and treatment of AS.

Background MicroRNA‐34a (miR‐34a) plays an essential role in regulating blood lipid, inflammation, cell adhesion molecules, and atherosclerosis, the latter factors are closely involved in the etiology of coronary heart disease (CHD). However, the clinical value of miR‐34a in CHD patients' management is rarely reported. Hence, this study aimed to assess the correlation of miR‐34a with disease risk, blood lipid, coronary artery stenosis, inflammatory cytokines, and cell adhesion molecules of CHD. Methods A total of 203 CHD patients and 100 controls were recruited in this study, then their plasma samples were collected to detect the miR‐34a by reverse transcription quantitative polymerase chain reaction. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecule measurement by enzyme‐linked immunosorbent assay. Results MiR‐34a was elevated in CHD patients compared to controls (p < 0.001) and it disclosed a good diagnostic value of CHD (area under curve: 0.899, 95% confidence interval: 0.865–0.934). Besides, miR‐34a positively correlated with triglyceride (p < 0.001), total cholesterol (p = 0.022) and low‐density lipoprotein cholesterol (p = 0.004), but not with high‐density lipoprotein cholesterol (p = 0.110) in CHD patients. Moreover, miR‐34a associated with Gensini score in CHD patients (p < 0.001). As to inflammation‐related indexes and cell adhesion molecules, MiR‐34a expression was positively linked with C‐reactive protein (p < 0.001), tumor necrosis factor alpha (p = 0.005), interleukin (IL)‐1β (p = 0.020), IL‐17A (p < 0.001), vascular cell adhesion molecule‐1 (p < 0.001), and intercellular adhesion molecule‐1 (p = 0.010) in CHD patients, but not with IL‐6 (p = 0.118) and IL‐10 (p = 0.054). Conclusion MiR‐34a might serve as a biomarker in assistance of diagnosis and management of CHD.

Background Brain‐derived neurotrophic factor (BDNF) exerts protective roles against dyslipidemia, atherosclerosis, and inflammation in cardiovascular diseases; meanwhile, it retards CD4+ T cell differentiation into T helper (Th)1 and Th17 cells. Hence, this study aimed to investigate the linkage of serum BDNF with Th1/Th2 ratio, Th17/regulatory T (Treg) ratio, and major adverse cardiovascular events (MACE) risk in the coronary heart disease (CHD) patients. Methods This prospective study detected serum BDNF in 210 CHD patients, 50 disease controls (DCs), and 50 healthy controls (HCs) using an enzyme‐linked immunosorbent assay. For CHD patients only, the proportion of Th1, Th2, Th17, and Treg cells in blood CD4+ T cells was calculated by flow cytometry. Results The BDNF varied among CHD patients, DC, and HC (p < 0.001). Specifically, BDNF was declined in CHD patients compared with DCs (p < 0.001) and HCs (p < 0.001). In CHD patients, BDNF was negatively related to Th1 cells (p = 0.031), Th1/Th2 ratio (p = 0.026), Th17 cells (p = 0.001), and Th17/Treg ratio (p = 0.002). Concerning the prognosis, BDNF was reduced in patients with MACE occurrence compared to patients without MACE occurrence (p = 0.006). Furthermore, BDNF showed a trend (lacked statistical significance) to relate to longer MACE‐free survival (p = 0.059). Besides, BDNF was related to the absence of obesity (p = 0.019), decreased total cholesterol (p = 0.043), low‐density lipoprotein cholesterol (p = 0.019), C‐reactive protein (p = 0.012), and Gensini score (p = 0.005). Conclusion Serum BDNF negatively correlates with Th1/Th2 ratio, Th17/Treg ratio, and estimates lower MACE risk in CHD patients.

Objective Long non‐coding RNA KQT‐like subfamily, member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) could regulate lipid metabolism, vascular smooth muscle cell function, inflammation, and atherosclerosis. This study aimed to evaluate whether lncRNA KCNQ1OT1 could serve as a biomarker for reflecting coronary heart disease (CHD) patients' disease situation and prognosis. Methods LncRNA KCNQ1OT1 expression was determined in peripheral blood mononuclear cells from 267 CHD patients, 50 disease controls (DCs) (unexplained chest pain), and 50 healthy controls (HCs) by the RT‐qPCR method. TNF‐α, IL‐17A, VCAM‐1, and ICAM‐1 were determined by the ELISA procedure in serum from CHD patients only. The mean (95% confidential interval) follow‐up duration was 16.0 (15.3–16.8) months. Results LncRNA KCNQ1OT1 was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). LncRNA KCNQ1OT1 could distinguish the CHD patients from DCs (area under the curve [AUC]: 0.757) and from the HCs (AUC: 0.880). LncRNA KCNQ1OT1 was positively associated with triglyceride (p = 0.026), low‐density lipoprotein cholesterol (p = 0.023), cardiac troponin I (p = 0.023), and C‐reactive protein (p = 0.001). Besides, lncRNA KCNQ1OT1 was also positively linked with the Gensini score (p = 0.008). Furthermore, lncRNA KCNQ1OT1 was positively related to the TNF‐α (p < 0.001), IL‐17A (p = 0.008), and VCAM‐1 (p = 0.003). LncRNA KCNQ1OT1 was elevated in CHD patients with MACE compared to those without MACE (p = 0.006); moreover, lncRNA KCNQ1OT1 high was associated with shorter MACE‐free survival (p = 0.018). Conclusion Circulating lncRNA KCNQ1OT1 expression not only reflects the stenosis degree, blood lipid level, and inflammation status but also predicts the MACE risk, while a large‐scale study is needed for verification.