[Retracted] Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway.

[This retracts the article DOI: 10.3892/etm.2016.

miR-487b mitigates chronic heart failure through inhibition of the IL-33/ST2 signaling pathway.

We investigated the effects of microRNA-587b (miR-487b) in a rat model of chronic heart failure (CHF). Wistar rats were assigned to 10 groups (n=8 per group). Expression of interleukin-33 (IL-33), somatostatin 2 (ST2), IL-6, and TNF-α was higher in the CHF group than the control group.

miR-26b-5p regulates hypoxia-induced phenotypic switching of vascular smooth muscle cells via the TGF-β/Smad4 signaling pathway.

Hypoxia contributes to the phenotypic switch of vascular smooth muscle cells (VSMCs). Various microRNAs (miRNAs) participate in this process as post‑transcriptional regulators, however the mechanism remains unclear. In the present study, mouse VSMCs (mVSMCs) harvested from aortas were cultured in normoxic and hypoxic conditions, and the mRNA levels of miR-26b-5p, desmin, H‑caldesmon and smoothelin were quantified using reverse transcription‑quantitative polymerase chain reaction.

Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF-β1/TAK1 signaling pathway.

Pharmacological postconditioning using cardioprotective agents is able to reduce myocardial infarct size. Notoginsenoside R1 (NG-R1), a phytoestrogen isolated from saponins (PNS), is considered to have anti-oxidative and anti-apoptotic properties. However, its cardioprotective properties and underlying mechanisms remain largely unknown.

Prevalence and Spectrum of TBX5 Mutation in Patients with Lone Atrial Fibrillation.

Atrial fibrillation (AF), the most common type of cardiac rhythm disturbance encountered in clinical practice, is associated with substantially increased morbidity and mortality. Aggregating evidence demonstrates that abnormal cardiovascular development is involved in the pathogenesis of AF. A recent study has revealed that the TBX5 gene, which encodes a T-box transcription factor key to cardiovascular development, was associated with AF and atypical Holt-Oram syndrome.

miR-146b-5p promotes VSMC proliferation and migration.

Vascular smooth muscle cells (VSMCs) play pivotal roles in the development of vascular diseases. While microRNAs are important in vascular pathologies, a few is known about their functional roles in VSMC phenotypes. We profiled microRNA expression in PDGF-BB treated VSMCs and found microRNA-146b-5p (miR-146b-5p) was upregulated.

miR-103 Regulates Oxidative Stress by Targeting the BCL2/Adenovirus E1B 19 kDa Interacting Protein 3 in HUVECs.

Oxidative stress plays a critical role in cardiovascular diseases. Salidroside, a glycoside from Rhodiola rosea, has been used as an antioxidative therapy for oxidative injury in cardiac diseases. However, the mechanism underlying its antioxidant effect needs to be elucidated.

Effects of GRK5 and ADRB1 polymorphisms influence on systolic heart failure.

Background: G-protein receptor kinase 5 (GRK5) Gln41 > Leu and β1-adrenergic receptor (ADRB1) Arg389 > Gly polymorphisms presented the different distribution of genotype frequencies between Caucasian American and African American, and produced the difference in β-blocker treatment effect among them with systolic heart failure (SHF).

Objective: This study sought to identify the distributed characteristics of these variant genotypes in Chinese population, and influence of GRK5 and ADRB1 polymorphisms on SHF morbidity and β-blocker treatment effect in patients with SHF.

Methods: This study was based on cross-sectional survey data.

Endothelial progenitor cells and atherosclerosis.

Atherosclerosis is due to inflammation and endothelial dysfunction and damage caused by a variety of factors. Dysfunction of endothelial progenitor cells (EPCs) that differentiate into mature endothelial cell contributes to the development of atherosclerosis. Both the number and functionality of EPCs are regulated, particularly in vascular repair.