Circular RNAs Regulate Vascular Remodelling in Pulmonary Hypertension.

Circular RNAs (circRNAs) are a newly identified type of noncoding RNA molecule with a unique closed-loop structure. circRNAs are widely expressed in different tissues and developmental stages of many species, participating in many important pathophysiological processes and playing an important role in the occurrence and development of diseases. This article reviews the discovery, characteristics, formation, and biological function of circRNAs.

Regulation of circular RNAs act as ceRNA in a hypoxic pulmonary hypertension rat model.

To explore potential critical genes and identify circular RNAs (circRNAs) that act as the competitive endogenous RNA (ceRNA) in a hypoxic pulmonary hypertension (HPH) rat model. Constructed rat model, and a bioinformatics method was used to analyse differentially expressed (DE) genes and construct a circRNA-miRNA-mRNA ceRNA regulatory network. Then, qRT-PCR was used to verify.

PDGF mediates pulmonary arterial smooth muscle cell proliferation and migration by regulating NFATc2.

The reconstruction of pulmonary vascular structure caused by the proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs) is the central link in the formation of pulmonary arterial hypertension (PAH). Platelet‑derived growth factor (PDGF) can regulate the proliferation and migration of PASMCs. At the same time, nuclear factor of activated T cells (NFATs) plays an important role in the development of PAH.

Comparison of the Clinical Characteristics and Severity of Influenza and Non-influenza Respiratory Virus-Related Pneumonia in China: A Multicenter, Real-World Study.

Purpose: Respiratory viruses are important etiologies of community-acquired pneumonia (CAP). However, the impact of different RVs on the outcomes of CAP is not well elucidated. This study aims to compare the clinical features and severity of influenza (Flu-p) and non-influenza respiratory viruses-related pneumonia (NIRVs-p) onset in the community among immunocompetent adults.

Correlation between DNA methylation and Thymic Stromal Lymphopoietin expression in asthmatic airway epithelial cells.

Background: The overexpression of TSLP and DNA methylation in asthma were both risk factors the relationship was not clear.

Objective: This study aimed to investigate the relationship between methylation status of TSLP promoter and mRNA/protein expression in asthmatic airway epithelial cells.

Methods: Human bronchial epithelial cells were cultured in vitro and divided into: Control group, treated with PBS, model group, sensitized with LPS (10 μg/mL) for 12 h (37 °C, 5% CO).

Severity and outcomes of influenza-related pneumonia in type A and B strains in China, 2013-2019.

Background: Inconsistencies exist regarding the severity of illness caused by different influenza strains. The aim of this study was to compare the clinical outcomes of hospitalized adults and adolescents with influenza-related pneumonia (Flu-p) from type A and type B strains in China.

Methods: We retrospectively reviewed data from Flu-p patients in five hospitals in China from January 2013 to May 2019.

MicroRNA-214-3p Regulates Hypoxia-Mediated Pulmonary Artery Smooth Muscle Cell Proliferation and Migration by Targeting ARHGEF12.

BACKGROUND miR-214-3p has been found to inhibit proliferation and migration in cancer cells. The objective of this study was to determine whether ARHGEF12 is involved in miR-214-3p-mediated suppression of proliferation and migration of pulmonary artery smooth muscle cells (PASMCs). MATERIAL AND METHODS PASMCs were cultured under normoxia or hypoxia.

5-Aza-2'-deoxycytidine, a DNA methylation inhibitor, attenuates hypoxic pulmonary hypertension via demethylation of the PTEN promoter.

Phosphatase and tensin homolog (PTEN) plays an important role in the pathogenesis of hypoxic pulmonary hypertension (HPH). A decrease in PTEN expression is associated with the hypermethylation of its promoter. However, whether the demethylation of the PTEN gene could attenuate HPH remains unknown.

Autophagy in pulmonary hypertension: Emerging roles and therapeutic implications.

Autophagy is an important mechanism for cellular self-digestion and basal homeostasis. This gene- and modulator-regulated pathway is conserved in cells. Recently, several studies have shown that autophagic dysfunction is associated with pulmonary hypertension (PH).

Serum cardiac troponin elevation predicts mortality in patients with pulmonary hypertension: A meta-analysis of eight cohort studies.

Objective: To determine the association of serum cardiac troponin (cTn) with the mortality of pulmonary hypertension (PH) patients via a meta-analysis.

Date Source: We searched PubMed and EMBASE from inception to October 25, 2017.

Study Selection: The reference lists of the retrieved articles were also consulted.

Sphingosine kinase 1/sphingosine 1-phosphate signalling pathway as a potential therapeutic target of pulmonary hypertension.

Pulmonary hypertension is characterized by extensive vascular remodelling, leading to increased pulmonary vascular resistance and eventual death due to right heart failure. The pathogenesis of pulmonary hypertension involves vascular endothelial dysfunction and disordered vascular smooth muscle cell (VSMC) proliferation and migration, but the exact processes remain unknown. Sphingosine 1-phosphate (S1P) is a bioactive lysophospholipid involved in a wide spectrum of biological processes.

Atorvastatin reduces lipopolysaccharide-induced expression of C-reactive protein in human lung epithelial cells.

Accumulating evidence suggests that statins possess anti-inflammatory properties and may decrease C-reactive protein (CRP) levels in plasma. However, no studies have as yet addressed whether or not statins regulate the expression of CRP in human lung epithelial cells (A549). In this study, we determined whether atorvastatin modulates the lipopolysaccharide (LPS)-induced expression of CRP in A549 cells.

Rho-kinase as a potential therapeutic target for the treatment of pulmonary hypertension.

Pulmonary hypertension (PH) is a cardiovascular disorder characterized by vasoconstriction and vascular remodeling. Recently, rapidly increasing evidence from various rat models of PH and patients with PH suggest that small GTPase Rho and its downstream effector, Rho-kinase, play a key role in the pathogenesis of PH. Activation of the Rho/Rho-kinase pathway is important for pulmonary endothelial dysfunction, pulmonary vascular smooth muscle cell contractility, proliferation and apoptosis in PH.

Statins may ameliorate pulmonary hypertension via RhoA/Rho-kinase signaling pathway.

Statins are the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors that function as potent inhibitors of cholesterol biosynthesis and have been used for many years for the treatment of hypercholesterolemia. However, accumulating experimental and clinical studies have revealed that the health benefits associated with statins treatment, particularly those conferred on the cardiovascular system, were the cholesterol-independent. Because statins inhibit an early step in the cholesterol biosynthetic pathway, they also inhibit the synthesis of isoprenoids such as farnesylpyrophosphate and geranylgeranylpyrophosphate, which are important postranslational lipid attachments for intracellular signaling molecules such as the Rho GTPases.