ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024
PAI-1 deficiency drives pulmonary vascular smooth muscle remodeling and pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 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
- Paradigm shift: from pulmonary vasodilation to cardiopulmonary dual-track therapy-a comprehensive review of pathophysiology and advances in pulmonary hypertension-associated right heart failure.Respiratory research · 2026Review
- Advances in the Research of Hypoxia-Inducible Factor-1Alpha and Plasminogen Activator Inhibitor-1 in Vascular-Related Diseases.Journal of clinical medicine research · 2026Review
- Immunological coagulation dual axis stratification identifies ultra high-risk phenotypes in systemic sclerosis.Frontiers in immunology · 2026Article
- Sepsis induces the cardiomyocyte apoptosis and cardiac dysfunction through activation of YAP1/Serpine1/caspase-3 pathway.Open medicine (Warsaw, Poland) · 2024Article
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Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vasoconstriction and remodeling of small pulmonary arteries (PAs). Central to the remodeling process is a switch of pulmonary vascular cells to a proliferative, apoptosis-resistant phenotype. Plasminogen activator inhibitors-1 and -2 (PAI-1 and PAI-2) are the primary physiological inhibitors of urokinase-type and tissue-type plasminogen activators (uPA and tPA), but their roles in PAH are unsettled. Here, we report that:
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