ReviewWorld journal of gastroenterology2010
Heme oxygenase-1 as a therapeutic target in inflammatory disorders of the gastrointestinal tract.
Review in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 58 citations in OpenAlex.
- The toxic footprint of lead exposure: oxido-inflammatory biomarkers in urban populations of Niger Delta, Nigeria.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Anti-inflammatory and anti-allergic potential of liquiritin extracted from Glycyrrhiza glabra L. in asthma management.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Effects of albiflorin on oxidative stress and inflammatory responses in rats with acute spinal cord injury.Immunity, inflammation and disease · 2023Article
- Combination of Niclosamide and Pirfenidone Alleviates Pulmonary Fibrosis by Inhibiting Oxidative Stress and MAPK/Nf-κB and STATs Regulated Genes.Pharmaceuticals (Basel, Switzerland) · 2023Article
- The different facets of heme-oxygenase 1 in innate and adaptive immunity.Cell biochemistry and biophysics · 2022Review
- Recent Insights into the Pathogenesis of Acute Porphyria Attacks and Increasing Hepatic PBGD as an Etiological Treatment.Life (Basel, Switzerland) · 2022Review
- A novel circular RNA, circIgfbp2, links neural plasticity and anxiety through targeting mitochondrial dysfunction and oxidative stress-induced synapse dysfunction after traumatic brain injury.Molecular psychiatry · 2022Article
- Regulation of Nrf2 and NF-κB activities may contribute to the anti-inflammatory mechanism of xylopic acid.Inflammopharmacology · 2022Article
- Kuwanon T and Sanggenon a Isolated fromMolecules (Basel, Switzerland) · 2021Article
- Suppression of Mitochondria-Related Bioenergetics Collapse and Redox Impairment by Tanshinone I, a Diterpenoid Found in Salvia miltiorrhiza Bunge (Danshen), in the Human Dopaminergic SH-SY5Y Cell Line Exposed to Chlorpyrifos.Neurotoxicity research · 2021Article
- New Class of Anti-Inflammatory Therapeutics Based on Gold (III) Complexes in Intestinal Inflammation-Proof of Concept Based on In Vitro and In Vivo Studies.International journal of molecular sciences · 2021Article
- Interdependence of Anti-Inflammatory and Antioxidant Properties of Squalene-Implication for Cardiovascular Health.Life (Basel, Switzerland) · 2021Review
- Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia.Frontiers in bioengineering and biotechnology · 2021Review
- A Multiple-Hit Hypothesis Involving Reactive Oxygen Species and Myeloperoxidase Explains Clinical Deterioration and Fatality in COVID-19.International journal of biological sciences · 2021Review
- Induction of HO-1 by Mevastatin Mediated via a Nox/ROS-Dependent c-Src/PDGFRα/PI3K/Akt/Nrf2/ARE Cascade Suppresses TNF-α-Induced Lung Inflammation.Journal of clinical medicine · 2020Article
- 5-Aminolevulinic acid regulates the immune response in LPS-stimulated RAW 264.7 macrophages.BMC immunology · 2018Article
- Article
- Alleviated mucosal and neuronal damage in a rat model of Crohn's disease.World journal of gastroenterology · 2014Article
- Heme oxygenase-1 ameliorates dextran sulfate sodium-induced acute murine colitis by regulating Th17/Treg cell balance.The Journal of biological chemistry · 2014Article
- Restoration of type I interferon expression by heme and related tetrapyrroles through inhibition of NS3/4A protease.The Journal of infectious diseases · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heme oxygenase (HO)-1 is the inducible isoform of the first and rate-limiting enzyme of heme degradation. HO-1 not only protects against oxidative stress and apoptosis, but has received a great deal of attention in recent years because of its potent anti-inflammatory functions. Studies with HO-1 knockout animal models have led to major advances in the understanding of how HO-1 might regulate inflammatory immune responses, although little is known on the underlying mechanisms. Due to its beneficial effects the targeted induction of this enzyme is considered to have major therapeutic potential for the treatment of inflammatory disorders. This review discusses current knowledge on the mechanisms that mediate anti-inflammatory protection by HO-1. More specifically, the article deals with the role of HO-1 in the pathophysiology of viral hepatitis, inflammatory bowel disease, and pancreatitis. The effects of specific HO-1 modulation as a potential therapeutic strategy in experimental cell culture and animal models of these gastrointestinal disorders are summarized. In conclusion, targeted regulation of HO-1 holds major promise for future clinical interventions in inflammatory diseases of the gastrointestinal tract.
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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.