ArticleCardiovascular research2014
NO-independent stimulation or activation of soluble guanylyl cyclase during early reperfusion limits infarct size.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Cardiovascular Effects of Stimulators of Soluble Guanylate Cyclase Administration: A Meta-analysis of Randomized Controlled Trials.Current atherosclerosis reports · 2024Pooled it
- Membrane-bound guanylyl cyclase-G deficiency impairs nitric oxide-mediated epithelial repair in intestinal ischemia-reperfusion injury in male mice.Scientific reports · 2026Article
- The Role of Vericiguat in Heart Failure Therapy: From Clinical Trials to Clinical Practice.Reviews in cardiovascular medicine · 2025Review
- Vericiguat: A Promising Drug for the Treatment of Heart Failure.Current cardiology reviews · 2025Review
- Review
- Bibliometric study of soluble guanylate cyclase stimulators in cardiovascular research based on web of science from 1992 to 2021.Frontiers in pharmacology · 2022Article
- cGMP at the centre of attention: emerging strategies for activating the cardioprotective PKG pathway.Basic research in cardiology · 2018Review
- Obestatin regulates cardiovascular function and promotes cardioprotection through the nitric oxide pathway.Journal of cellular and molecular medicine · 2017Article
- Cardioprotective effects of PKG activation by soluble GC activator, BAY 60-2770, in ischemia-reperfusion-injured rat hearts.PloS one · 2017Article
- BAY 41-2272 Treatment Improves Acetylcholine-Induced Aortic Relaxation in L-NAME Hypertensive Rats.The International journal of angiology : official publication of the International College of Angiology, Inc · 2016Article
- Soluble guanylate cyclase activation during ischemic injury in mice protects against postischemic inflammation at the mitochondrial level.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Widening and Elaboration of Consecutive Research into Therapeutic Antioxidant Enzyme Derivatives.Oxidative medicine and cellular longevity · 2016Review
- Postconditioning signalling in the heart: mechanisms and translatability.British journal of pharmacology · 2015Review
- The cGMP/PKG pathway as a common mediator of cardioprotection: translatability and mechanism.British journal of pharmacology · 2015Review
- Vasorelaxing effects of the soluble guanylyl cyclase activator BAY 60-2770 in nitrate-tolerant monkey and canine coronary arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsGuanylyl cyclase-cyclic guanosine monophosphate signalling plays an important role in endogenous cardioprotective signalling. The aim was to assess the potential of direct pharmacological activation and stimulation of soluble guanylyl cyclase, targeting different redox states of the enzyme, to limit myocardial necrosis during early reperfusion. METHODS AND
resultsRat isolated hearts were subjected to reversible left coronary artery occlusion (ischaemia-reperfusion) and infarct size was assessed by the tetrazolium staining technique. Administration during early reperfusion of BAY 41-2272, an NO-independent, haem-dependent stimulator of soluble guanylyl cyclase targeting the reduced state, or BAY 60-2770, an NO-independent, haem-independent activator targeting the oxidized state, significantly limited infarct size. Inhibition of NO synthesis did not abrogate this protection, but exogenous perfusion of NO with BAY 41-2272 produced a synergistic effect. The haem site oxidiser, ODQ abrogated the protection afforded by BAY 41-2272 but potentiated the protection afforded by BAY 60-2770. Targeting both the reduced and oxidized forms of sGC together did not afford additive protection.
conclusionsTargeting either reduced or oxidized forms of sGC during early reperfusion affords cardioprotection, providing support for the concept that direct sGC manipulation at reperfusion has therapeutic potential for the management of acute myocardial infarction.
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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.