ArticleNature communications2025
Macrophage ferroptosis potentiates GCN2 deficiency induced pulmonary venous arterialization.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Alkylating Agent-Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The integrated stress response kinase GCN2 prevents ZAKα-Dependent inflammatory hyperactivation in macrophages.The Journal of biological chemistry · 2026Article
- Interleukin-6 is critical in the development of pulmonary vascular disease inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Therapeutic Targets for Pediatric Pulmonary Vein Stenosis: Insights from Animal Models.Children (Basel, Switzerland) · 2026Review
- Neutrophil Irgm1 ameliorates sepsis-induced myocardial dysfunction by promoting Alox15 degradation.Redox biology · 2026Article
- PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4.Redox biology · 2026Article
- Huaier Aqueous Extract Combined with Gefitinib Promotes ACSL4-Dependent Ferroptosis and Overcomes Gefitinib Resistance in Non-Small Cell Lung Cancer.Current medical science · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Pulmonary veno-occlusive disease (PVOD) is a fatal disease characterized by the remodelling of pulmonary veins and haemosiderin accumulation in macrophages. Although (General Control Nonderepressible 2) GCN2 deficiency has been reported in PVOD patients, the underlying mechanism by which GCN2 deficiency affects the pulmonary venous cells and the surrounding cells, remains unclear. Here, we perform immunohistochemistry and scRNA-sequencing analyses to show that macrophages are the major population affected by GCN2 deficiency and ferroptosis pathway-related genes are upregulated in lung macrophages of PVOD patients. Treatment with the specific ferroptosis inhibitor ferrostatin-1 (Fer-1) reverses the changes in haemodynamic indices observed in Eif2ak4
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