ArticleCanadian respiratory journal2026
The Role and Mechanism of HIF-1α in Regulating A549 Alveolar Epithelial Cell Function Under Hypoxic Conditions.
Article in Canadian respiratory journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- The Role and Mechanism of HIF-1α in Regulating A549 Alveolar Epithelial Cell Function Under Hypoxic Conditions.Canadian respiratory journal · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aims to investigate the regulatory role and mechanism of hypoxia-inducible transcription Factor 1 (HIF-1α) in alveolar epithelial cell function under hypoxic conditions using A549 cells as a surrogate model. Methods: Human A549 alveolar epithelial cells were used as the experimental model. HIF-1α expression was modulated by siRNA knockdown or plasmid overexpression. qRT-PCR quantified HIF-1α, SP-C, and vascular endothelial growth factor (VEGF) mRNA levels, and Western blotting evaluated the corresponding proteins and apoptosis-related markers (cleaved Caspase 3, Bcl-2, Bax). Cell counting kit 8 (CCK-8) assessed A549 cell viability, while transwell assays measured migration (uncoated membrane) and invasion (Matrigel-coated membrane). Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining detected the apoptosis. Enzyme-linked immunosorbent assay (ELISA) quantified VEGF secretion, and tube-formation assays evaluated the proangiogenic effects of A549-conditioned media on human umbilical vein endothelial cells (HUVECs). Results: Hypoxia markedly increased HIF-1α and VEGF expression while reducing SP-C expression in A549 cells. HIF-1α knockdown decreased VEGF expression and angiogenesis, restored cell viability, and suppressed migration, invasion, and apoptosis. In contrast, HIF-1α overexpression further enhanced angiogenesis, promoted migration and invasion, and increased apoptosis. Conclusions: HIF-1α is a key regulator of hypoxia-induced functional changes in alveolar epithelial cells, influencing cell viability, migration, invasion, apoptosis, VEGF production, and proangiogenic activity. These findings highlight their potential as a therapeutic target in hypoxia-related lung injury.
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Registered trials
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