ArticlePurinergic signalling2011
The carbon monoxide donor, CORM-2, is an antagonist of ATP-gated, human P2X4 receptors.
Article in Purinergic signalling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Slow Releasing CO Donor Modulates Susceptibility to Seizures in Rats with Chronic Prostatitis/Chronic Pelvic Pain Syndrome: Behavioral and EEG Study.Medicina (Kaunas, Lithuania) · 2025Article
- Compelling Evidence: A Critical Update on the Therapeutic Potential of Carbon Monoxide.Medicinal research reviews · 2025Review
- Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.International journal of molecular sciences · 2024Review
- On the Question of CO's Ability to Induce HO-1 Expression in Cell Culture: A Comparative Study Using Different CO Sources.ACS chemical biology · 2024Article
- Recent progress on anti-nociceptive effects of carbon monoxide releasing molecule-2 (CORM-2).Molecular and cellular biochemistry · 2024Review
- Plight of CORMs: The unreliability of four commercially available CO-releasing molecules, CORM-2, CORM-3, CORM-A1, and CORM-401, in studying CO biology.Biochemical pharmacology · 2023Review
- Sensing a CO-Releasing Molecule (CORM) Does Not Equate to Sensing CO: The Case of DPHP and CORM-3.Analytical chemistry · 2023Article
- Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018Review
- Carbon Monoxide-Releasing Molecule-2 Inhibits Connexin 43-Hemichannel Activity in Spinal Cord Astrocytes to Attenuate Neuropathic Pain.Journal of molecular neuroscience : MN · 2017Article
- Blockade of P2X4 Receptors Inhibits Neuropathic Pain-Related Behavior by Preventing MMP-9 Activation and, Consequently, Pronociceptive Interleukin Release in a Rat Model.Frontiers in pharmacology · 2017Article
- CORM-2 inhibits TXNIP/NLRP3 inflammasome pathway in LPS-induced acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- CO-releasing Metal Carbonyl Compounds as Antimicrobial Agents in the Post-antibiotic Era.The Journal of biological chemistry · 2015Review
- Diverse mechanisms underlying the regulation of ion channels by carbon monoxide.British journal of pharmacology · 2015Review
- Pharmacological activation of heme oxygenase (HO)-1/carbon monoxide pathway prevents the development of peripheral neuropathic pain in Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Carbon monoxide reduces neuropathic pain and spinal microglial activation by inhibiting nitric oxide synthesis in mice.PloS one · 2012Article
- Therapeutic potential of heme oxygenase-1/carbon monoxide in lung disease.International journal of hypertension · 2012Article
- Carbon monoxide: an emerging regulator of ion channels.The Journal of physiology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbon monoxide (CO) is produced endogenously by heme oxygenase (HO) enzymes. HO-1 is highly expressed in many inflammatory disease states, where it is broadly protective. The protective effects of HO-1 expression can be largely mimicked by the exogenous application of CO and CO-releasing molecules (CORMs). Despite a dearth of pharmacological tools for their study, molecular methodologies have identified P2X4 receptors as a potential anti-nociceptive drug target. P2X4 receptors are up-regulated in animal models of inflammatory pain, and their knock-down reduces pain behaviours. In these same animal models, HO-1 expression is anti-nociceptive, and we therefore investigated whether P2X4 was a target for CO and tricarbonyldichlororuthenium (II) dimer (CORM-2). Using conventional whole-cell and perforated-patch recordings of heterologously expressed human P2X4 receptors, we demonstrate that CORM-2, but not CO gas, is an inhibitor of these channels. We also investigated the role of soluble guanylate cyclase and mitochondria-derived reactive oxygen species using pharmacological inhibitors but found that they were largely unable to affect the ability of CORM-2 to inhibit P2X4 currents. A control breakdown product of CORM-2 was also without effect on P2X4. These results suggest that P2X4 receptors are not a molecular target of endogenous CO production and are, therefore, unlikely to be mediating the anti-nociceptive effects of HO-1 expression in inflammatory pain models. However, these results show that CORM-2 is an effective antagonist at human P2X4 receptors and represents a useful pharmacological tool for the study of these receptors given the current dearth of antagonists.
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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.