Src family kinases (SFKs) is a non-receptor protein tyrosine kinases family. They are crucial in signal transduction and regulation of various cell biological processes, such as proliferation, differentiation and apoptosis. The role and mechanism of SFKs in tumorigenesis have been widely studied. However, more and more studies have also shown that SFKs are involved in the pathogenesis of pulmonary fibrosis (PF). Myofibroblasts activation, epithelial-mesenchymal transition and inflammation response are three pivotal pathomechanisms in the development of pulmonary fibrotic disease. In this article, we summarize the roles of SFKs in these biological processes. SFKs play a crucial role in the pathogenesis of PF, making it a promising molecular target for the treatment of these diseases. We will pay special attention to the role of SFKs in idiopathic pulmonary fibrosis (IPF), and also emphasize the important findings in other pulmonary fibrotic diseases because their pathological mechanisms are similar. We will then describe the translation results obtained with SFKs inhibitors in basic and clinical studies.

The objective of this study was to explore the neuroprotective effect of moxibustion on rats with Parkinson’s disease (PD) and its mechanism. A Parkinson’s disease model was established in rats using a two-point stereotactic 6-hydroxydopamine injection in the right substantia nigra (SN) and ventral tegmental area. The rats received moxibustion at the Baihui (GV20) and Sishencong (EX-HN1) acupoints for 20 minutes, six times a week, for 6 weeks. The right SN tissue was histologically and immunohistochemically examined. Differentially expressed genes (DEGs) were identified through RNA sequencing. In addition, the levels of tyrosine hydroxylase (TH), glutathione peroxidase 4 (GPX4), and ferritin heavy chain 1 (FTH1) in SN were measured. In comparison to the model group, the moxibustion group showed a significantly greater TH immunoreactivity and a higher behavioural score. In particular, moxibustion led to an increase in the number and morphological stability of SN neural cells. The functional pathway analysis showed that DEGs are closely related to the ferroptosis pathway. GPX4 and FTH1 in the SN were significantly overexpressed in the moxibustion-treated rats with PD. Moxibustion can effectively reduce the death of SN neurons, decrease the occurrence of ferroptosis, and increase the TH activity to protect the neurons in rats with PD. The protective mechanism may be associated with suppression of the ferroptosis.

More and more clinical trials have tried to assess the clinical benefit of anti-interleukin (IL)-13 monoclonal antibodies for uncontrolled asthma. The aim of this study is to evaluate the efficacy and safety of anti-IL-13 monoclonal antibodies for uncontrolled asthma. Major databases were searched for randomized controlled trials comparing the anti-IL-13 treatment and a placebo in uncontrolled asthma. Outcomes, including asthma exacerbation rate, forced expiratory volume in 1 second (FEV₁), Asthma Quality of Life Questionnaire (AQLQ) scores, rescue medication use, and adverse events were extracted from included studies for systematic review and meta-analysis. Five studies involving 3476 patients and two anti-IL-13 antibodies (lebrikizumab and tralokinumab) were included in this meta-analysis. Compared to the placebo, anti-IL-13 treatments were associated with significant improvement in asthma exacerbation, FEV₁ and AQLQ scores, and reduction in rescue medication use. Adverse events and serious adverse events were similar between two groups. Subgroup analysis showed patients with high periostin level had a lower risk of asthma exacerbation after receiving anti-IL-13 treatment. Our study suggests that anti-IL-13 monoclonal antibodies could improve the management of uncontrolled asthma. Periostin may be a good biomarker to detect the specific subgroup who could get better response to anti-IL-13 treatments. In view of blocking IL-13 alone is possibly not enough to achieve asthma control because of the overlapping pathophysiological roles of IL-13/IL-4 in inflammatory pathways, combined blocking of IL-13 and IL-4 with monoclonal antibodies may be more encouraging.

Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) are highly prevalent potential risk factors for systemic disease. Previous studies have reported that COPD and OSA are major independent risk factors for cardio‑ or cerebrovascular diseases. The present study aimed to investigate the role of bone marrow mesenchymal stem cells (BMSCs) on vascular injury in a COPD‑OSA overlap syndrome (OS) rat model. Rats were randomly divided into three groups: Sham, OS model and BMSC. BMSC localization in major organs was detected via confocal laser fluorescence microscopy, and the aortic tissue pathological changes and related genes were measured using hematoxylin & eosin and Masson staining. Genes associated with vascular endothelial cell injury, including endothelin 1, vascular cell adhesion molecule 1 and endothelial nitric oxide synthase, were detected via reverse transcription‑quantitative PCR and western blotting. Apoptosis of vascular endothelial cells was detected using TUNEL and immunofluorescence assays. The endothelial cell marker CD31 in injured vessels was analyzed via immunohistochemistry. BMSCs migrated into the heart, liver, spleen, lung, kidney, brain and aorta in the OS model. The green fluorescence expression of BMSCs demonstrated the highest level in the lung, followed by the aorta. Aortic tissue had a more severe vascular injury and increased apoptosis in the model group compared with the BMSC group. Vascular endothelial cell apoptosis was decreased in the BMSC group compared with the model group. The findings suggested that BMSCs could repair vascular injury by inhibiting endothelial cell damage and apoptosis. These data provide a theoretical basis for the treatment of cardiovascular diseases caused by OS with BMSCs.