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Air pollution can lead to many cardiovascular and respiratory diseases, but the impact of air pollution on pulmonary embolism is still uncertain. We conducted a meta-analysis to assess the relationship between air pollution and pulmonary embolism. We searched PubMed, EMBASE, Web of Science, and the Cochran Library for citations on air pollutants (carbon monoxide, sulfur dioxide, nitrogen dioxide, ozone and particulate matter) and pulmonary embolism. A total of nine citations met the inclusion criteria. There is no evidence of bias. CO, SO2, PM10 and PM2.5 had no significant effect on the occurrence of pulmonary embolism. NO2 and O3 can increase the risk of pulmonary embolism to a small extent. This meta-analysis suggests that some air pollutants are associated with an increased risk of pulmonary embolism. Reducing air pollution and improving air quality can effectively reduce the risk of pulmonary embolism. [ABSTRACT FROM AUTHOR]

Bone marrow mesenchymal stem cells (BMMSCs) are used in cardiac tissue engineering for the regeneration of diseased hearts. We examined the differentiation of rat BMMSCs into cardiomyocyte-like cells when induced with a combined low dose treatment of transforming growth factor-β1 (TGF-β1) and 5-azacytidine (5-AZA). Results showed that cell proliferation in the combined low dose treatment group of TGF-β1 and 5-AZA was increased compared with the TGF-β1 group or the 5-AZA group. The cell apoptosis was relieved by combined TGF-β1 and 5-AZA treatment compared to 5-AZA treatment alone. The number of cells positive for myosin heavy chain, connexin-43, α-actin, and troponin I in the combined treatment group was higher than those observed in the TGF-β1 group or the 5-AZA group. Moreover, the combined low dose treatment group of TGF-β1 and 5-AZA reveals the strongest expression of troponin I, α-actin, and phosphorylated extracellular signal-regulated protein kinases 1 and 2 (p-ErK1/2) among the treatment groups. These results suggest that the combined low dose treatment of TGF-β1 and 5-AZA can improve the differentiation potential of rat BMMSCs into cardiomyocyte-like cells and alleviate cell damage effects in vitro. The mechanism that is involved in influencing differentiation may be associated with p-ErK1/2. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to address inconsistencies in results between the H9C2 myocardial hypoxia (MH) cell line and myocardial infarction (MI) rat models used in MI research. We identified differentially expressed genes (DEGs) and underlying molecular mechanisms using RNA sequencing technology., Methods: RNA sequencing was used to analyse DEGs in MI rat tissues and H9C2 cells exposed to hypoxia for 24 h. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to identify key biological processes and pathways. Weighted correlation network analysis [weighted gene co-expression network analysis (WGCNA)] was used to construct gene co-expression networks, and hub genes were compared with published MI datasets [Gene Expression Omnibus (GEO)] for target identification., Results: GO analysis revealed enrichment of immune inflammation and mitochondrial respiration processes among 5139 DEGs in MI tissues and 2531 in H9C2 cells. KEGG analysis identified 537 overlapping genes associated with metabolism and oxidative stress pathways. Cross-analyses using the published GSE35088 and GSE47495 datasets identified 40 and 16 overlapping genes, respectively, with nine genes overlapping across all datasets and our models. WGCNA identified a key module in the MI model enriched for mRNA processing and protein binding. GO analysis revealed enrichment of mRNA processing, protein binding and mitochondrial respiratory chain complex I assembly in MI and H9C2 MH models. Five relevant hub genes were identified via a cross-analysis between the 92 hub genes that showed a common expression trend in both models., Conclusions: This study reveals both shared and distinct transcriptomic responses in the MI and H9C2 models, highlighting the importance of model selection for studying myocardial ischaemia and hypoxia., (© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)