ReviewCells2022
Hypoxia-Inducible Factor Signaling in Inflammatory Lung Injury and Repair.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- [Natural bear bile powder attenuates lipopolysaccharide-induced acute lung injury in mice by regulating the NF-κB and Nrf-2/HO-1 signaling pathways].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Digital twins of ex vivo human lungs enable accurate and personalized evaluation of therapeutic efficacy.Nature biotechnology · 2026Article
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.Immunity, inflammation and disease · 2026Article
- Lactate dehydrogenase-to-albumin ratio as a potential prognostic indicator in glucocorticoid-treated severe pneumonia: a multicenter retrospective study with external validation.Frontiers in immunology · 2026Article
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- Article
- Decoding fibrosis in nonresolvable COVID-19: a role for myeloid-specific HIF1A deletion.American journal of physiology. Cell physiology · 2025Article
- Hypoxia-Inducible Factor 1-alpha (HIF1α), Nicotinamide Adenine Dinucleotide (NAD+, NADH), and Nitric Oxide (NO) interplay in critically ill patients, with implications for patient safety and targeted therapies: a review.Patient safety in surgery · 2025Review
- Review
- Correlation of METTL4 genetic variants and severe pneumonia pediatric patients in Southern China.BMC genomic data · 2025Article
- Role of Hypoxia-Inducible Factors in Respiratory Syncytial Virus Infection-Associated Lung Disease.International journal of molecular sciences · 2025Article
- Hypoxia Imaging in Lung Cancer: A PET-Based Narrative Review for Clinicians and Researchers.Pharmaceuticals (Basel, Switzerland) · 2025Review
- SERPINE1 maintained expression by NR4A1 promotes invasion and migration of glioblastoma in hypoxic microenvironment.Frontiers in oncology · 2025Article
- AIDET communication combined with alternating prone ventilation for HIF-1α, sTREM-1 and hs-CRP in awake elderly patients with severe pneumonia.Frontiers in medicine · 2025Article
- Expression and Regulation of Hypoxia-Inducible Factor Signalling in Acute Lung Inflammation.Cells · 2024Review
- New Insights into Aspirin's Anticancer Activity: The Predominant Role of Its Iron-Chelating Antioxidant Metabolites.Antioxidants (Basel, Switzerland) · 2024Review
- Hypoxia-inducible-factors differentially contribute to clinical disease and viral replication during RSV infection.bioRxiv : the preprint server for biology · 2024Article
- Atractylodin modulates ASAH3L to improve galactose metabolism and inflammation to alleviate acute lung injury.iScience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Inflammatory lung injury is characterized by lung endothelial cell (LEC) death, alveolar epithelial cell (AEC) death, LEC-LEC junction weakening, and leukocyte infiltration, which together disrupt nutrient and oxygen transport. Subsequently, lung vascular repair is characterized by LEC and AEC regeneration and LEC-LEC junction re-annealing, which restores nutrient and oxygen delivery to the injured tissue. Pulmonary hypoxia is a characteristic feature of several inflammatory lung conditions, including acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and severe coronavirus disease 2019 (COVID-19). The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs) 1 and 2. These transcription factors control the expression of a wide variety of target genes, which in turn mediate key pathophysiological processes including cell survival, differentiation, migration, and proliferation. HIF signaling in pulmonary cell types such as LECs and AECs, as well as infiltrating leukocytes, tightly regulates inflammatory lung injury and repair, in a manner that is dependent upon HIF isoform, cell type, and injury stimulus. The aim of this review is to describe the HIF-dependent regulation of inflammatory lung injury and vascular repair. The review will also discuss potential areas for future study and highlight putative targets for inflammatory lung conditions such as ALI/ARDS and severe COVID-19. In the development of HIF-targeted therapies to reduce inflammatory lung injury and/or enhance pulmonary vascular repair, it will be vital to consider HIF isoform- and cell-specificity, off-target side-effects, and the timing and delivery strategy of the therapeutic intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.