Cardiac fibrosis is the pathological consequence of fibroblast proliferation and fibroblast-to-myofibroblast transition. As a new class of endogenous non-coding RNAs, circular RNAs (circRNAs) have been identified in many cardiovascular diseases including fibrosis, generally acting as microRNA (miRNA) sponges. Here, we report that the expression of circRNA–circNFIB was decreased in mice post-myocardial infarction heart samples, as well as in primary adult cardiac fibroblasts treated with TGF-β. Forced expression of circNFIB decreased cell proliferation in both NIH/3T3 cells and primary adult fibroblasts as evidenced by EdU incorporation. Conversely, inhibition of circNFIB promoted adult fibroblast proliferation. Furthermore, circNFIB was identified as a miR-433 endogenous sponge. Overexpression of circNFIB could attenuate pro-proliferative effects induced by the miR-433 mimic while inhibition of circNFIB exhibited opposite results. Finally, upregulation of circNFIB also reversed the expression levels of target genes and downstream signaling pathways of miR-433. In conclusion, circNFIB is critical for protection against cardiac fibrosis. The circNFIB–miR-433 axis may represent a novel therapeutic approach for treatment of fibrotic diseases.

Membrane structure design is critical for the development of high-performance hemodialysis membranes. Here, a thin-film nanofibrous composite (TFNC) membrane, consisting of a two-tier composite structure, i.e., an ultrathin hydrophilic separation layer of chemically cross-linked polyvinyl alcohol (PVA), and an electrospun polyacrylonitrile (PAN) nanofibrous supporting layer, was demonstrated as the hemodialysis membrane for the first time. The optimized PVA/PAN TFNC membrane exhibited high permeability (~ 290.5 L/m 2 h at 0.1 MPa) and excellent selectivity which should be attributed to its unique structure with ultrathin separation layer and highly porous supporting layer. In addition, the TFNC membrane also possessed excellent overall mechanical properties, good hydrophilicity and comparable hemocompatibility properties (protein adsorption, platelet adhesion, complement activation, hemolysis ratio). The hemodialysis simulation experiments on optimized TFNC membrane showed that 82.6% of urea and 45.8% of lysozyme were cleaned and 98.8% of bovine serum albumin (BSA) was retained. The TFNC membranes exhibited excellent hemodialysis performances, especially for the middle-molecule uremic toxin removal, which was more efficient than conventional hemodialysis membranes reported so far, suggesting PVA/PAN TFNC membranes as promising alternatives for hemodialysis applications.

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Cardiac hypertrophy is classified as pathological and physiological hypertrophy. Pathological hypertrophy typically precedes the onset of heart failure, one of the largest contributors to disease burden and deaths worldwide. In contrast, physiological hypertrophy is an adaptive response and protects against adverse cardiac remodeling. Noncoding RNAs (ncRNAs) have drawn significant attention over the last couple of decades, and their dysregulation is increasingly being linked to cardiac hypertrophy and cardiovascular diseases. In this review, we will summarize the profiling, function, and molecular mechanism of microRNAs, long noncoding RNAs, and circular RNAs in pathological cardiac hypertrophy. Additionally, we also review microRNAs responsible for physiological hypertrophy. With better understanding of ncRNAs in cardiac hypertrophy, manipulation of the important ncRNAs will offer exciting avenues for the prevention and therapy of heart failure.

Acute myocardial infarction (AMI) represents a leading cause of morbidity and mortality worldwide. Extracellular vesicles (EVs) are being recognized as a promising therapeutic approach in protecting against MI. Serum is a rich source of EVs, which transports various microRNAs (miRNAs, miRs). EVs from serum have been shown beneficial for protecting against ischemia-reperfusion injury; however, their roles in AMI are unclear. In addition, whether a miRNA might be responsible for the effects of serum EVs on protecting against AMI is undetermined. Here, we demonstrated that serum EVs significantly reduced cardiomyocytes apoptosis in both cellular and mouse models of AMI, and dramatically attenuated the infarct size in mouse hearts after AMI. Inhibition of miR-21 was shown to reduce the protective effects of serum EVs in inhibiting cardiomyocytes apoptosis. miR-21 was decreased in mouse hearts after AMI, while serum EVs increased that. In addition, the programmed cell death 4 (PDCD4) expression was identified as a target gene of miR-21. Therefore, our study showed the protective effects of serum EVs on AMI, and provided a novel strategy for AMI therapy.

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