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. To the best of our knowledge, there are no reports yet regarding whether PDGF regulates NFATc2 to increase the proliferation of PASMCs. The present study aimed to investigate whether PDGF affects the proliferation and migration of PASMCs by regulating NFAT, and to study the pathogenesis of PAH. PASMCs were treated with recombinant PDGF; Cell Counting Kit‑8 and clone formation experiments showed that PDGF enhanced the cell viability and proliferation of PASMCs. Cell cycle distribution and molecular markers related to cell proliferation (cyclin D1, CDK4 and Proliferating Cell Nuclear Antigen) were detected by flow cytometry, and the results indicated that PDGF promoted the division of PAMSCs. The scratch migration and Transwell migration assays showed that the migratory ability of PASMCs was enhanced following PDGF treatment. Changes in NFATs (NFATc1‑5) after PDGF treatment were evaluated by reverse transcription‑quantitative PCR and western blotting; NFATc2 showed the most significant results. Finally, PDGF‑treated cells were treated with an NFAT pathway inhibitor, cyclosporin A, or a small interfering RNA targeting NFATc2, and changes in cell proliferation and migration were evaluated to assess the role of NFATc2 in PDGF‑induced cell proliferation and migration. In conclusion, PDGF may regulate PASMC proliferation and migration by regulating the expression of NFAT, further leading to the occurrence of PAH. It is proposed that NFATc2 could be used as a potential target for PAH treatment.

Objectives Patients with pulmonary embolism (PE) have a higher red cell distribution width (RDW), which may complicate the interpretation of the prognosis of PE. We aim to evaluate the diagnostic utility of the RDW in patients with PE. Methods Eligible studies were identified by searching PubMed and EMBASE from inception to December 23, 2018. The data were pooled using Stata 12 to evaluate the prognostic value. The sources of heterogeneity were detected. Results For the analysis of prognosis, 7 studies with 2146 patients were included, with median RDW values ranging from 13.4% to 15.7% and a median cut-off point of 18.27%. A total of 247 patients (11.5% mortality) among the 2146 participants died. Overall, RDW was positively associated with the prognosis of PE in the overall analysis (HR = 1.19, 95% CI = 1.10-1.29,I-2 = 73.4%;P = 0.000). Subgroup analyses by study design, sex and follow-up time indicated that they were not sources of heterogeneity. Conclusions An elevated RDW has the potential to be a biomarker for prognosis in PE patients.

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. The Q test and I² test were used for to assess heterogeneity. The relationship between cTn elevation and mortality was analysed. Studies were stratified according to type of troponin (cTnT vs cTnI), region (Europe vs America) and follow‐up length (≤3 years vs >3 years).Results: Eight studies with 739 patients were included in the meta‐analysis. Cardiac troponin elevation ranged from 14.3% to 94.5%. Overall, 48.8% (39/80) of patients with elevated cTn died compared to 18.6% (45/242) of patients with normal cTn levels. These findings showed cTn elevation was significantly related to an increased mortality risk in PH patients [hazard ratio (HR) = 3.05, 95% confidence interval (95% CI) = 2.16‐4.32, I² = 24.9%]. cTnI was better at predicting mortality than cTnT (HR = 3.37, 95%CI = 2.05‐5.55 vs HR = 2.80, 95%CI = 1.97‐3.98, respectively). American populations had increased mortality compared to European populations (HR = 4.23, 95%CI = 2.29‐7.80 vs HR = 2.70, 95% CI = 1.95‐3.74, respectively). This finding was independent of the follow‐up length of the studies (≤3 years: HR = 2.36, 95%CI = 1.65‐3.38; >3 years: HR = 4.55, 95%CI = 2.80‐7.39).Conclusions: Although different studies detected the expression cTnT or cTnI by various methods, the mortality in the cTn‐positive group was higher than that in the cTn‐negative group. Serum cTn elevation emerged as an independent predictor of increased risk of mortality in PH patients.

Oxidative stress is an imbalance between the body’s reactive oxygen species and antioxidant defense mechanisms. Oxidative stress is involved in the development of several cardiovascular diseases, such as pulmonary hypertension, atherosclerosis, and diabetes mellitus. A growing number of studies have suggested the potential role of oxidative stress in the pathogenesis of pulmonary embolism. Biomarkers of oxidative stress in pulmonary embolism have also been explored, such as matrix metalloproteinases, asymmetric dimethylarginine, and neutrophil/lymphocyte ratio. Here, we comprehensively summarize some oxidative stress mechanisms and biomarkers in the development of acute pulmonary embolism and summarize related treatments based on antioxidant stress to explore effective treatment strategies for acute pulmonary embolism.