ArticleBMC cardiovascular disorders2024
β-catenin mediates monocrotaline-induced pulmonary hypertension via glycolysis in rats.
Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Review
- Lactate and Lactylation in Respiratory Diseases: from Molecular Mechanisms to Targeted Strategies.Lung · 2025Review
- Positive association between serum lactate dehydrogenase levels and blood pressure: evidence from NHANES 2015-2016.Frontiers in cardiovascular medicine · 2025Article
- Macrophage-driven immunopathology in pulmonary arterial hypertension: from mechanisms to targeted therapies.Frontiers in immunology · 2025Review
- Natural products targeting the immune-metabolic regulatory network in pulmonary hypertension: mechanisms, classification, and therapeutic prospects.Frontiers in pharmacology · 2025Review
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7 authors.
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Abstract
backgroundMetabolic abnormalities and immune inflammation are deeply involved in pulmonary vascular remodelling and the development of pulmonary hypertension (PH). However, the regulatory mechanisms of glycolysis in macrophages are still elusive. Cumulative evidence indicates that β-catenin plays a crucial role in metabolic reprogramming. This study aimed to investigate the effect of β-catenin on macrophage glycolysis in PH.
methodsLPS-induced BMDMs were generated via in vitro experiments. A monocrotaline (MCT)-induced PH rat model was established, and the β-catenin inhibitor XAV939 was administered in vivo. The role of β-catenin in glycolysis was analysed. The degree of pulmonary vascular remodelling was measured.
resultsβ-catenin was significantly increased in both in vitro and in vivo models. In LPS-induced BMDMs, β-catenin increased the levels of hexokinase 2 (HK2), phosphofructokinase (PFK), M2-pyruvate kinase (PKM2), lactate dehydrogenase (LDH), and lactate (LA) and the expression of inflammatory cytokines and promoted PASMC proliferation and migration in vitro. XAV939 decreased the level of glycolysis and downregulated the expression of inflammatory cytokines in vivo. MCT promoted pulmonary arterial structural remodelling and right ventricular hypertrophy, and XAV939 alleviated these changes.
conclusionsOur findings suggest that β-catenin is involved in the development of PH by promoting glycolysis and the inflammatory response in macrophages. Inhibition of β-catenin could improve the progression of PH.
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