ArticlePoultry science2021
Dysregulated expression of mRNA and SNP in pulmonary artery remodeling in ascites syndrome in broilers.
Article in Poultry science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Broiler Ascites Syndrome as a Potential Spontaneous Animal Model for Human Pulmonary Arterial Hypertension: A Narrative Review.Life (Basel, Switzerland) · 2026Review
- A novel traditional Chinese medicine compound alleviates broiler ascites syndrome by modulating the IL-6/STAT3/FOXO3a signaling pathway.Poultry science · 2026Article
- Changes in the Expression of MIF and Other Key Enzymes of Energy Metabolism in the Myocardia of Broiler Chickens with Ascites Syndrome.Animals : an open access journal from MDPI · 2022Article
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Authors and funding
14 authors.
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Abstract
Broiler ascites syndrome (AS), also called pulmonary artery hypertension, is a metabolic disorder that has been observed worldwide in fast-growing broilers. Pulmonary arterial remodeling is a key step in the development of AS. The precise relationship between mRNA and SNP of the pulmonary artery in regulating AS progression remains unclear. In this study, we obtained pulmonary artery tissues from broilers with AS to perform pathologic section and pathologic anatomic observation. SNP, InDel, and mRNA data analysis were carried out using GATK and ANNOVAR software to study the SNP loci of 985 previously reported genes (437 upregulated and 458 downregulated). The pathology results showed that there was a lot of yellow fluid in the abdominal cavity and pericardium, that the ascites cardiac index and hematocrit changed significantly, and that the pulmonary artery had remodeled and become thicker in the disease group. Myocardial sections showed vacuolar degeneration of myocytes and rupture of muscle fibers. In addition, ALDH7A1, IRG1, GGT5, IGSF1, DHX58, USP36, TREML2, SPAG1, CD34, and PLEKHA7 were found to be closely associated with the pathogenesis of pulmonary artery remodeling in AS progression. Taken together, our present study further illuminates the molecular mechanism of pulmonary artery remodeling underlying AS progression.
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