Cardiovascular diseases (CVDs) remain the world’s leading cause of death. Cardiomyocyte autophagy helps maintain normal metabolism and functioning of the heart. Importantly, mounting evidence has revealed that autophagy plays a dual role in CVD pathology. Under physiological conditions, moderate autophagy maintains cell metabolic balance by degrading and recycling damaged organelles and proteins, and it promotes myocardial survival, but excessive or insufficient autophagy is equally deleterious and contributes to disease progression. Noncoding RNAs (ncRNAs) are a class of RNAs transcribed from the genome, but most ncRNAs do not code for functional proteins. In recent years, increasingly, various ncRNAs have been identified, and they play important regulatory roles in the physiological and pathological processes of organisms, as well as in autophagy. Thus, determining whether ncRNA-regulated autophagy plays a protective role in CVDs or promotes their progression can help us to develop ncRNAs as therapeutic targets in autophagy-related CVDs. In this review, we briefly summarize the regulatory roles of several important ncRNAs, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the autophagy of various CVDs to provide a theoretical basis for the etiology and pathogenesis of CVDs and develop novel therapies to treat CVDs.

Cardiovascular disease (CVD) is one of the most important diseases endangering human life. The pathogenesis of CVDs is complex. Pyroptosis, which differs from traditional apoptosis and necrosis, is characterized by cell swelling until membrane rupture, resulting in the release of cell contents and activation of a strong inflammatory response. Recent studies have revealed that inflammation and pyroptosis play important roles in the progression of CVDs. Noncoding RNAs (ncRNAs) are considered promising biomarkers and potential therapeutic targets for the diagnosis and treatment of various diseases, including CVDs. Growing evidence has revealed that ncRNAs can mediate the transcriptional or posttranscriptional regulation of pyroptosis-related genes by participating in the pyroptosis regulatory network. The role and molecular mechanism of pyroptosis-regulating ncRNAs in cardiovascular pathologies are attracting increasing attention. Here, we summarize research progress on pyroptosis and the role of ncRNAs, particularly microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the regulation of pyroptosis in CVD pathologies. Identifying these disease-related ncRNAs is important for understanding the pathogenesis of CVDs and providing new targets and ideas for their prevention and treatment.

Anti-mitochondrial antibodies, the hallmark of primary biliary cirrhosis, have been detected in many patients with idiopathic inflammatory myopathies and these anti-mitochondrial-antibody-associated idiopathic inflammatory myopathies frequently show unique characteristics. We detected anti-mitochondrial antibodies in Chinese idiopathic inflammatory myopathy and summarized the clinical findings of these anti-mitochondrial-antibody-positive patients. Of 136 patients, seven (5.15%) were found to be anti-mitochondrial-antibody-positive. Primary biliary cirrhosis was present in 2 of these 7 patients, chronic disease duration in 2 patients and asymmetrical muscle weakness in 4 patients. The mean disease course was 8.58 months, and the mean creatine kinase level was 2256.53 U/L. Myositis-specific antibodies were found in 3 patients. According to clinical features and muscle histopathological findings, 3 patients were classified as dermatomyositis, 2 as possible polymyositis and 2 as necrotizing autoimmune myopathy. Of the 6 anti-mitochondrial-antibody-positive patients receiving follow-ups of 12-83 months, they all showed marked clinical improvement. Our study indicates that anti-mitochondrial antibodies are relatively rare in Chinese idiopathic inflammatory myopathy patients. These patients generally show various clinical features and have favorable treatment outcomes. Anti-mitochondrial antibody testing may be helpful to confirm the diagnosis of idiopathic inflammatory myopathy, especially in patients with atypical manifestations.

The higher prevalence of metabolic syndrome (MetS) in women after menopause is associated with a decrease in circulating 17β-oestradiol. To explore novel treatments for MetS in women with oestrogen deficiency, we studied the effect of exogenous butyrate on diet-induced obesity and metabolic dysfunctions using ovariectomized (OVX) mice as a menopause model. Oral administration of sodium butyrate (NaB) reduced the body fat content and blood lipids, increased whole-body energy expenditure, and improved insulin sensitivity. Additionally, NaB induced oestrogen receptor alpha (ERα) expression, activated the phosphorylation of AMPK and PGC1α, and improved mitochondrial aerobic respiration in cultured skeletal muscle cells. In conclusion, oral NaB improves metabolic parameters in OVX mice with diet-induced obesity. Oral supplementation with NaB might provide a novel therapeutic approach to treating MetS in women with menopause. Graphical Abstract