INTRODUCTION Atherosclerosis (AS), a chronic inflammatory disease of the arterial wall characterized by gradual build-up of arterial plaque, is the main cause of cardiovascular disease (CVD) [1, 2]. Aging is a major, independent risk factor for AS [3]. Macrophages are main components of the inflammatory plaque and promote AS development across its different stages [4-6]. Accumulating data indicates that pyroptosis, a highly inflammatory form of programmed cell death usually triggered in immune cells upon infection by intracellular pathogens, occurs also in AS-associated macrophages and contributes importantly to plaque instability [7, 8]. Therefore, therapies aimed at inhibiting macrophage pyroptosis may reduce the morbidity and mortality associated with AS.

Atherosclerosis is a chronic inflammatory disease that commonly affects the elderly and is characterized by vascular damage, macrophage infiltration, and plaque formation. Moreover, it increases the risk of cardiovascular disease. The pathogenesis of atherosclerosis involves an interplay between macrophage autophagy and apoptosis. A recently discovered transcription factor, transcription factor EB (TFEB) is known to activate autophagy in macrophages. Sirtuin deacetylase 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD + )-dependent histone deacetylase, activates several transcription factors, including TFEB. We studied the effects of berberine on the NAD + synthesis pathway and interactions between SIRT1 and TFEB. We also studied the effects of berberine-induced TFEB activation via SIRT1 on autophagy and apoptosis of peritoneal macrophages. We found that berberine promoted autophagy of peritoneal macrophages by activating SIRT1 via the NAD + synthesis pathway and, in turn, promoting TFEB nuclear translocation and deacetylation. The functional regulation of SIRT1 and TFEB by berberine could be exploited as a potential therapeutic strategy for atherosclerosis.

Atherosclerosis, predominantly characterized by the disturbance of lipid homeostasis, has become the main causation of various cardiovascular diseases. Therefore, there is an urgent requirement to explore efficacious targets that act as lipid modulators for atherosclerosis. Transcription factor EB (TFEB), whose activity depends on post-translational modifications, such as phosphorylation, acetylation, SUMOylation, ubiquitination, etc., is significant for normal cell physiology. Recently, increasing evidence implicates a role of TFEB in lipid homeostasis, via its functionality of promoting lipid degradation and efflux through mediating lipophagy, lipolysis, and lipid metabolism-related genes. Furthermore, a regulatory effect on lipid transporters and lipid mediators by TFEB is emerging. Notably, TFEB makes a possible therapeutic target of atherosclerosis by regulating lipid metabolism. This review recapitulates the update and current advances on TFEB mediating lipid metabolism to focus on two intracellular activities: a) how cells perceive external stimuli and initiate transcription programs to modulate TFEB function, and b) how TFEB restores lipid homeostasis in the atherosclerotic process. In-depth research is warranted to develop potent agents against TFEB to alleviate or reverse the progression of atherosclerosis.

Atherosclerosis (AS) is a chronic inflammatory disease seriously endangering human health, whose occurrence and development is related to many factors. Pyroptosis is a recently identified novel programmed cell death associated with an inflammatory response and involved in the formation and progression of AS by activating different signaling pathways. Protein modifications of the sirtuin family and microRNAs (miRNAs) can directly or indirectly affect pyroptosis-related molecules. It is important to link atherosclerosis, thermogenesis and molecular modifications. This article will systematically review the molecular pathways of pyroptosis in AS, which can provide a new perspective for AS prevention and treatment.

Ischemic heart disease (IHD) is a considerable health burden worldwide with high mortality and morbidity. Treatments for IHD are mainly focused on decreasing oxygen demand or increasing myocardial oxygen supply, including pharmacological, interventional, and surgical treatment, but there are also some limitations. Therefore, it is important to find a simple, effective, and economical treatment. As non-invasive and safe physiotherapy, electrical stimulation (ES) has a promising application in the treatment of IHD. Current studies suggest that ES can affect the occurrence and development of IHD by promoting angiogenesis, regulating autophagy and apoptosis, inhibiting the inflammatory response and oxidative stress. In this review, we focus predominantly on the mechanism of ES and the current progress of ES therapy in IHD, furthermore, give a brief introduction to the forms of ES in clinical application.