ArticleJournal of thoracic disease2025
miR-124/PTBP1/PKM axis modulates pulmonary artery endothelial metabolism in a pulmonary thromboembolism rat model.
Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
- The diagnostic and short-term prognostic significance of miR-183-5p in pulmonary embolism and its regulation of disease progression through PDCD4.Clinical and experimental medicine · 2026Article
- Role of PKM2 Tetramer in Modulating Endothelial Mitochondrial Dysfunction in a Rat Model of Chronic Thromboembolic Pulmonary Hypertension.Physiological research · 2026Article
- Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cellular metabolism is critical for endothelial cell function. Pulmonary artery endothelial cell (PAEC) dysfunction contributes to the progression from pulmonary embolism (PE) to chronic thromboembolic pulmonary hypertension (CTEPH). The mechanisms of metabolic changes in PAECs during this progression remain unclear. This study aimed to explore the role of the miR-124/PTBP1/PKM signaling axis in endothelial metabolic reprogramming and pulmonary arterial intimal remodeling in pulmonary thromboembolism (PTE). Methods: A PTE rat model was established through repeated autologous thrombus injections into the external jugular veins. The miR-124 levels were restored using a miR-124 mimic, and pathological changes in the pulmonary arteries and thrombi were observed. The expression levels of PTBP1, PKM2, PKM1, MPC1, and MPC2 in the pulmonary arterial intima were assessed using immunohistochemistry, polymerase chain reaction (PCR), and western blotting. Biochemical methods were employed to measure blood lactate levels. Results: Compared to the normal control group, rats with PTE exhibited increased PTBP1 and PKM2 expression in the pulmonary arterial intima, while miR-124, PKM1, MPC1, and MPC2 expression levels were reduced. Overexpression of miR-124 lowered PTBP1 and PKM2 levels in the intima while elevating PKM1, MPC1, and MPC2 levels, ultimately leading to a reduction in lactic acid production. Conclusions: In the PTE rat model, elevated lactate levels, decreased miR-124 expression in the pulmonary arterial intima, and disrupted energy metabolism were observed. The miR-124/PTBP1/PKM signaling axis may play a role in the reprogramming of cell metabolism during chronic PTE, ultimately contributing to pulmonary arterial intimal remodeling.
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