Activated neutrophil membrane-coated tRF-Gly-CCC nanoparticles for the treatment of aortic dissection/aneurysm.

Aortic dissection/aneurysm (AAD) is a critical and life-threatening condition marked by a lack of effective pharmacological treatments. Gene therapy has emerged as a promising approach to treat AAD and slow its advancement. However, the clinical utility of gene therapy is impeded by significant challenges, including the scarcity of innovative genetic drugs in current medical practices and the absence of a streamlined gene delivery mechanism.

Targeting the KCa3.1 channel suppresses diabetes-associated atherosclerosis via the STAT3/CD36 axis.

Background: In diet-induced arterial atherosclerosis, increased KCa3.1 channel was associated with atherosclerotic plaque progression and instability. Macrophages are involved in the formation of atherosclerotic plaques, and the release of inflammatory cytokines and oxygen free radicals promotes plaque progression.

Identification of vital modules and genes associated with heart failure based on weighted gene coexpression network analysis.

Aims: Heart failure (HF) is a chronic heart disease with a high incidence and mortality. Due to the regulatory complexity of gene coexpression networks, the underlying hub genes regulation in HF remain incompletely appreciated. We aimed to explore potential key modules and genes for HF using weighted gene coexpression network analysis (WGCNA).

Comprehensive analysis of the ceRNA network in coronary artery disease.

With the rapid aging of the population, coronary artery disease (CAD) has become one of the most fatal chronic diseases. However, the genetic mechanism of CAD is still unclear. The purpose of this study is to construct the lncRNA-miRNA-mRNA regulatory network for CAD diseases and systematically identify differentially expressed genes in patients with coronary heart disease.

Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3β signalling pathway in diabetes mellitus.

Vascular dysfunction resulting from diabetes is an important factor in arteriosclerosis. Previous studies have shown that during hyperglycaemia and diabetes, AKAP150 promotes vascular tone enhancement by intensifying the remodelling of the BK channel. However, the interaction between AKAP150 and the BK channel remains open to discussion.

Effect of BIN1 on cardiac dysfunction and malignant arrhythmias.

Heart failure (HF) is the end-stage syndrome for most cardiac diseases, and the 5-year morbidity and mortality of HF remain high. Malignant arrhythmia is the main cause of sudden death in the progression of HF. Recently, bridging integrator 1 (BIN1) was discovered as a regulator of transverse tubule function and calcium signalling in cardiomyocytes.

Cardiac function modulation depends on the A-kinase anchoring protein complex.

The A-kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates.

Critical regulation of atherosclerosis by the KCa3.1 channel and the retargeting of this therapeutic target in in-stent neoatherosclerosis.

Coronary heart disease is a serious cardiovascular illness. Percutaneous coronary artery stent implantation has become a routine way to treat coronary heart disease. Although studies have shown how a drug-eluting stent could improve the efficacy of clinical treatment, 10~20% of in-stent restenosis is still an important outcome that restricts the clinical efficacy of drug-eluting stent implantations and causes cardiovascular events such as angina pectoris, acute myocardial infarction, and sudden death.

MicroRNA‑mRNA integrated analysis based on a case of well‑differentiated thyroid cancer with both metastasis and metastatic recurrence.

The incidence of well‑differentiated thyroid cancer (WDTC) is rapidly increasing. Poor survival follows distant metastasis (DM) and recurrence. In the present study, we aimed to analyze the expression alterations in different stages of WDTC and the regulatory mechanism of DM and the recurrence of DM.

Curcumin downregulates the expression of Snail via suppressing Smad2 pathway to inhibit TGF-β1-induced epithelial-mesenchymal transitions in hepatoma cells.

Hepatocellular carcinoma (HCC) remains the third cause of cancer-related mortality. Resection and transplantation are the only curative treatments available but are greatly hampered by high recurrence rates and development of metastasis, the initiation of cancer metastasis requires migration and invasion of cells, which is enabled by epithelial-mesenchymal transitions (EMT). TGF-β1 is a secreted protein that performs many cellular functions, including the control of cell growth, cell proliferation, cell differentiation and apoptosis.

[Cloning and expression of the succinate dehydrogenase iron-sulfur protein of Schistosoma japonicum Chinese strain in E. coli].

Objective: To clone the full-length gene encoding succinate dehydrogenase iron-sulfur protein of Schistosoma japonicum (SjSDISP) Chinese strain and express it in Escherichia coli.

Methods: According to the published incomplete EST (BU804141) of SjSDISP and the sequence of multiclone sites of lambda gt11 vector, 2 pairs of primers were designed and synthesized. Then the 3' and 5'ends of the EST of the SjSDISP from adult Schistosoma japonicum cDNA library were amplified by anchored PCR.