Role of pyroptosis in cardiovascular disease

Abstract

Cardiac function is determined by the dynamic equilibrium of various cell types and the extracellular matrix that composes the heart. Cardiovascular diseases (CVDs), especially atherosclerosis and myocardial infarction, are often accompanied by cell death and acute/chronic inflammatory reactions. Caspase-dependent pyroptosis is characterized by the activation of pathways leading to the activation of NOD-like receptors, especially the NLRP3 inflammasome and its downstream effector inflammatory factors interleukin (IL)-1β and IL-18. Many studies in the past decade have investigated the role of pyroptosis in CVDs. The findings of these studies have led to the development of therapeutic approaches based on the regulation of pyroptosis, and some of these approaches are in clinical trials. This review summarizes the molecular mechanisms, regulation and cellular effects of pyroptosis briefly and then discusses the current pyroptosis studies in CVD research.

Vildagliptin inhibits high free fatty acid (FFA)-induced NLRP3 inflammasome activation in endothelial cells

“…It should be noted that the pathological mechanisms of endothelial dysfunction are complicated and need to be further elucidated. Diverse risk factors, including genetics, aging, and obesity, are reported to be involved in cardiovascular disease [30]. Animal experimentation is an important method for exploring the pathogenesis and treatment of cardiovascular diseases.…”

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

“…As ABCA1 can regulate cholesterol metabolism and inflammation, indicating MEG3 could indirectly affect cholesterol metabolism and inflammation. It was shown that MEG3 enhanced pyroptosis, a highly inflammatory form of programmed cell death, in ox-LDL treated HCAECs by sponging miR-223 targeting NOD-like receptor protein 3 (NLRP3) (85,114). Consistently, MEG3 was upregulated in ox-LDL treated RAW264.7 cells and increased secretion of TNF-α and IL1β by sponging miR-204, which targeted the cyclin-dependent kinase inhibitor 2A (CDKN2A) (86).…”

The role of lncRNA MALAT1 in cardiovascular disease

“…Pyroptosis, a novel pro‐inflammatory programmed cell death process, participates in pathogenesis of CVD . MALAT1 promotes high glucose or ox‐LDL‐induced pyroptosis of ECs partly by affecting the expression of pyrin domain 3 (NRLP3) through competitively binding miR‐22 .…”

“…36 Conversely, some studies indicated that angiogenesis was also associated with the growth of atherosclerotic lesions and plaque destabilization. 37 Many studies showed that MALAT1 was largely induced in ECs and involved in the pathology of vascular diseases [29][30][31][32] (Table 1).…”