ArticleBritish journal of pharmacology2017
AP39, a mitochondria-targeting hydrogen sulfide (H
Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Pre- and postconditioning the heart with hydrogen sulfide (HBasic research in cardiology · 2018Pooled it
- Hydrogen Sulphide Signalling in Plants: From Persulfidation to Metabolic Regulation and Stress Response.Plant, cell & environment · 2026Review
- Hydrogen sulfide-mediated protein s-persulfidation: a regulatory mechanism in cardiovascular homeostasis.Molecular medicine (Cambridge, Mass.) · 2026Review
- Mitochondria-Targeted Hydrogen Sulphide Delivery via an Adhesive Hydrogel Modulates Inflammation and Oxidative Stress in Diabetic Wounds.Gels (Basel, Switzerland) · 2026Article
- NFS1 Regulates IDH2 to Attenuate Abdominal Aortic Aneurysms via Interacting With SP2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- AP39 alleviates HHCY-induced myocardial remodeling by regulating FUNDC1-mediated mitochondrial dynamics via S-sulfhydration of NEDD8/CUL4B.Frontiers in pharmacology · 2026Article
- Lipophilic Cations as Mitochondria-Targeting Moieties: Recent Progress and Design Principles for Medicinal Chemistry.Journal of medicinal chemistry · 2025Review
- Beyond Static Cold Storage: Toward the Next Generation of Tailored Organ Preservation Solutions.International journal of molecular sciences · 2025Review
- Precision Medicine: Therapeutically Targeting Mitochondrial Alterations in Heart Failure.JACC. Basic to translational science · 2025Review
- Mitochondrial targets in ischaemic heart disease and heart failure, and their potential for a more efficient clinical translation. A scientific statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardial Function.European journal of heart failure · 2025Review
- Epigenetics of Homocystinuria, Hydrogen Sulfide, and Circadian Clock Ablation in Cardiovascular-Renal Disease.Current issues in molecular biology · 2024Review
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- Effects and Mechanism of AP39 on Ovarian Functions in Rats Exposed to Cisplatin and Chronic Immobilization Stress.Journal of menopausal medicine · 2024Article
- Concurrent Subcellular Delivery of Hydrogen Sulfide and a Payload with Near-Infrared Light.JACS Au · 2024Article
- Pills of Multi-Target HInternational journal of molecular sciences · 2024Review
- Review
- AP39 through AMPK-ULK1-FUNDC1 pathway regulates mitophagy, inhibits pyroptosis, and improves doxorubicin-induced myocardial fibrosis.iScience · 2024Article
- Using mechanism-based combinations of HNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
background and purposeH EXPERIMENTAL APPROACH: Anaesthetized rats underwent myocardial ischaemia (30 min)/reperfusion (120 min) with randomization to receive interventions before reperfusion: vehicle, AP39 (0.01, 0.1, 1 μmol·kg KEY
resultsAP39, dose-dependently, reduced infarct size. Inhibition of either PI3K/Akt, eNOS or sGC did not affect this effect of AP39. Western blot analysis confirmed that AP39 did not induce phosphorylation of Akt, eNOS, GSK-3β or ERK1/2. In isolated subsarcolemmal and interfibrillar mitochondria, AP39 significantly attenuated mitochondrial ROS generation without affecting respiratory complexes I or II. Furthermore, AP39 inhibited mitochondrial permeability transition pore (PTP) opening and co-incubation of mitochondria with AP39 and cyclosporine A induced an additive inhibitory effect on the PTP. CONCLUSION AND IMPLICATIONS: AP39 protects against reperfusion injury independently of the cytosolic RISK pathway. This cardioprotective effect could be mediated by inhibiting PTP via a cyclophilin D-independent mechanism. Thus, selective delivery of H
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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.