ArticleAmerican journal of respiratory cell and molecular biology2022
Loss of cAbl Tyrosine Kinase in Pulmonary Arterial Hypertension Causes Dysfunction of Vascular Endothelial Cells.
Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Second- and Third-Generation BCR-ABL Tyrosine Kinase Inhibitors and the Risk of Pulmonary Arterial Hypertension: A Prevalent New-User Design.Circulation · 2026Article
- TRPC channels contribute to endothelial dysfunction in pulmonary arterial hypertension.Respiratory research · 2025Article
- Drugs and toxins associated with pulmonary arterial hypertension: from established culprits to novel threats.ERJ open research · 2025Review
- Dissecting Autophagy Gene Expression in Endothelial Cells of Pulmonary Arterial Hypertension at Single-Cell Resolution.Cardiology research · 2025Article
- Pharmacology and Rationale for Seralutinib in the Treatment of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Tyrosine Kinases and Endothelial Homeostasis in Pulmonary Arterial Hypertension: Too Hot to Handle?American journal of respiratory cell and molecular biology · 2022Article
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12 authors at 2 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a progressive and fatal disease characterized by the dysfunction of pulmonary endothelial cells (ECs) and obstructive vascular remodeling. cAbl (non-receptor tyrosine kinase c-Abelson) plays central roles in regulating cell-cycle arrest, apoptosis, and senescence after cellular stress. We hypothesized that cAbl is downactivated in experimental and human PAH, thus leading to reduced DNA integrity and angiogenic capacity of pulmonary ECs from patients with PAH (PAH-ECs). We found cAbl and phosphorylated cAbl concentrations to be lower in the endothelium of remodeled pulmonary vessels in the lungs of patients with PAH than in control subjects. Similar observations were obtained for the lungs of Sugen + hypoxia and monocrotaline rats with established pulmonary hypertension. These
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