ArticleRadiation research2019
12-Lipoxygenase is a Critical Mediator of Type II Pneumocyte Senescence, Macrophage Polarization and Pulmonary Fibrosis after Irradiation.
Article in Radiation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Methyl Quercetin Inhibits Radiation-induced Senescence and TGF-β1-induced Myofibroblast Differentiation Through psmad3/TGF-β Signaling.Radiation research · 2026Article
- NOX4 suppresses malignant progression in prostate adenocarcinoma and functions as a potential diagnostic biomarker.Translational andrology and urology · 2026Article
- Molecular mechanisms and network interactions in radiation-induced lung injury.Frontiers in physiology · 2026Review
- MIF/CD74 axis regulates alveolar epithelial type II cell apoptosis, autophagy, and transdifferentiation in bronchopulmonary dysplasia via the TGFβ1/SMAD4 pathway.Respiratory research · 2025Article
- Effects and potential mechanisms of the ultra-high dose rate radiotherapy on lung injury: a review.Radiation oncology (London, England) · 2025Review
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- Ferroptosis in pulmonary fibrosis: pathogenesis and traditional Chinese medicine-driven therapeutic approaches.Frontiers in cell and developmental biology · 2025Review
- Mitigating Viral Impact on the Radiation Response of the Lung.Radiation research · 2024Article
- The role of macrophage polarization and cellular crosstalk in the pulmonary fibrotic microenvironment: a review.Cell communication and signaling : CCS · 2024Review
- Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.American journal of physiology. Cell physiology · 2023Review
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- LINE-1 promotes tumorigenicity and exacerbates tumor progression via stimulating metabolism reprogramming in non-small cell lung cancer.Molecular cancer · 2022Article
- Article
- Biology of Radiation-Induced Lung Injury.Seminars in radiation oncology · 2021Review
- Effect of 3,3'-Diindolylmethane on Pulmonary Injury Following Thoracic Irradiation in CBA Mice.Health physics · 2020Article
- Radiotherapy Increases 12-LOX and CCL5 Levels in Esophageal Cancer Cells and Promotes Cancer Metastasis via THP-1-Derived Macrophages.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Radiation-induced pulmonary fibrosis (RIPF) is a chronic, progressive complication of therapeutic irradiation of the thorax. It has been suggested that senescence of type II pneumocytes (AECIIs), an alveolar stem cell, plays a role in the development of RIPF through loss of replicative reserve and via senescent AECII-driven release of proinflammatory and profibrotic cytokines. Within this context, we hypothesized that arachidonate 12-lipoxygenase (12-LOX) is a critical mediator of AECII senescence and RIPF. Treatment of wild-type AECIIs with 12S-hydroxyeicosateraenoic acid (12S-HETE), a downstream product of 12-LOX, was sufficient to induce senescence in a NADPH oxidase 4 (NOX4)-dependent manner. Mice deficient in 12-LOX exhibited reduced AECII senescence, pulmonary collagen accumulation and accumulation of alternatively activated (M2) macrophages after thoracic irradiation (5 × 6 Gy) compared to wild-type mice. Conditioned media from irradiated or 12S-HETE-treated primary pneumocytes contained elevated levels of IL-4 and IL-13 compared to untreated pneumocytes. Primary macrophages treated with conditioned media from irradiated AECII demonstrated preferential M2 type polarization when AECIIs were derived from wild-type mice compared to 12-LOX-deficient mice. Together, these data identified 12-LOX as a critical component of RIPF and a therapeutic target for radiation-induced lung injury.
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Registered trials
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