Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling.

Polystyrene microplastics (PS-MPs) are new types of environmental pollutant that have garnered significant attention in recent years since they were found to cause damage to the human respiratory system when they are inhaled. The pulmonary fibrosis is one of the serious consequences of PS-MPs inhalation. However, the impact and underlying mechanisms of PS-MPs on pulmonary fibrosis are not clear.

Cbx4 governs HIF-1α to involve in Th9 cell differentiation promoting asthma by its SUMO E3 ligase activity.

The potential role of polycomb chromobox 4 (Cbx4), as a small ubiquitin-like ligase (SUMO) E3 ligase, in the development and exacerbation of asthma remains unclear. Hypoxia inducible factor-1 (HIF-1) is a key transcription factor in the cellular response to hypoxia and contributes to the pathogenesis and progression of a range of diseases, including asthma. Here, we aimed to investigate the interaction of Cbx4 with Hypoxia inducible factor-1α (HIF-1α) and the potent mechanism of action in asthma progression.

Orai3 mediates Orai channel remodelling to activate fibroblast in pulmonary fibrosis.

Orai family are a calcium channel of cell membrane extracellular Ca influx which participates in tissue fibrosis. But the roles of Orai3 have less attention on the mechanism of regulating lung fibrosis. In this study, we found that Orai3 expression was increased significantly in BLM-induced lung fibrosis.

CBX4 Regulates Long-Form Thymic Stromal Lymphopoietin-mediated Airway Inflammation through SUMOylation in House Dust Mite-induced Asthma.

Thymic stromal lymphopoietin presents in two distinct isoforms: short-form (sfTSLP) and long-form (lfTSLP). lfTSLP promotes inflammation, whereas sfTSLP inhibits inflammation, in allergic asthma. However, little is known about the regulation of lfTSLP and sfTSLP during allergic attack in the asthma airway epithelium.

Short isoform thymic stromal lymphopoietin reduces inflammation and aerobic glycolysis of asthmatic airway epithelium by antagonizing long isoform thymic stromal lymphopoietin.

Background: Up-regulation of aerobic glycolysis has been reported as a characterization of asthma and facilitates airway inflammation. We has been previously reported that short isoform thymic stromal lymphopoietin (sTSLP) could reduce inflammation in asthmatic airway epithelial cells. Here we wanted to investigate whether the inhibition of sTSLP on asthma is related to aerobic glycolysis.

Long non-coding RNA TUG1 promotes airway remodeling and mucus production in asthmatic mice through the microRNA-181b/HMGB1 axis.

MicroRNA-181b (miR-181b) has been well noted with anti-inflammatory properties in several pathological conditions. It has also been suggested to be downregulated in patients with asthma. In this study, we explored the function of miR-181b in airway remodeling in asthmatic mice and the molecular mechanism.

High-mobility group box 1 impairs airway epithelial barrier function through the activation of the RAGE/ERK pathway.

Recent studies have indicated that high-mobility group box 1 protein (HMGB1) and the receptor for advanced glycation end-products (RAGE) contribute to the pathogenesis of asthma. However, whether the activation of the HMGB1/RAGE axis mediates airway epithelial barrier dysfunction remains unknown. Thus, the aim of this study was to examine the effects of HMGB1 and its synergistic action with interleukin (IL)-1β on airway epithelial barrier properties.

[Effect of microbubble cavitation on microcirculation of rat skeletal muscle].

Objective: To investigate the effect of therapeutic ultrasound-induced microbubble destruction on the microcirculation of rat skeletal muscle.

Methods: Thirty SD rats were randomized into 5 groups (n=6), namely normal saline, microbubble, ultrasound, high-energy ultrasound microbubble and low-energy ultrasound microbubble groups. Before and after the treatments, the diameter and blood flow velocity in the microvessels in the skeletal muscle were measured, and the structural changes of the injured microvessels observed by electron microscopy.