ReviewFrontiers in immunology2022
A Dual Role of Heme Oxygenase-1 in Tuberculosis.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- A single-cell atlas of peripheral immunity suggests immune subset attrition during tuberculosis dissemination.The Journal of international medical research · 2026Article
- Carbon monoxide-producing probioticiScience · 2026Article
- Characterization of the Effect of α-Lipoic Acid in Human Macrophages Infected withInternational journal of molecular sciences · 2026Article
- HowVaccines · 2026Review
- LncRNA-CFTBS enhancesVirulence · 2025Article
- Heme in Bacterial Pathogenesis and as an Antimicrobial Target.Chemical reviews · 2025Review
- Ferroptosis: molecular mechanisms, pathophysiology, and role in pediatric pulmonary diseases.Cell biology and toxicology · 2025Review
- Host-directed therapeutic targets in macrophages and their ligands against mycobacteria tuberculosis.Infection and immunity · 2025Review
- Heme and immunity: The heme oxygenase dichotomy.Journal of inorganic biochemistry · 2025Review
- Identification of ferroptosis-related key genes in tuberculosis by bioinformatics methods.AMB Express · 2025Article
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- ELAVL1-dependent SOAT2 exacerbated the pancreatitis-like cellular injury of AR42J cells induced by hyperstimulation with caerulein.The Kaohsiung journal of medical sciences · 2025Article
- Redox Biomarkers in Asymptomatic Latent Human Tuberculosis: A Comparison With Active Disease.The Journal of infectious diseases · 2024Article
- Crosstalk between ferroptosis and macrophages: potential value for targeted treatment in diseases.Molecular and cellular biochemistry · 2024Review
- Targeting Bacteria-Induced Ferroptosis of Bone Marrow Mesenchymal Stem Cells to Promote the Repair of Infected Bone Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Plasma metabolomic analysis reveals the metabolic characteristics and potential diagnostic biomarkers of spinal tuberculosis.Heliyon · 2024Article
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line.Frontiers in public health · 2024Article
- The influence of microbiota on ferroptosis in intestinal diseases.Gut microbes · 2023Review
- A human lung alveolus-on-a-chip model of acute radiation-induced lung injury.Nature communications · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron metabolism is vital for the survival of both humans and microorganisms. Heme oxygenase-1 (HO-1) is an essential stress-response enzyme highly expressed in the lungs, and catabolizes heme into ferrous iron, carbon monoxide (CO), and biliverdin (BV)/bilirubin (BR), especially in pathological conditions which cause oxidative stress and inflammation. Ferrous iron (Fe
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.