ReviewJournal of molecular and cellular cardiology2014
Monoamine oxidases as sources of oxidants in the heart.
Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 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.
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Who cites it
122 citing papers in PubMed, 241 citations in OpenAlex.
- Synthesis of 1,2,4-Oxadiazole Sulfonamide Derivatives and Their Biological Investigation as Monoamine Oxidase Inhibitors.Molecules (Basel, Switzerland) · 2026Article
- Nicotine-containing products and the cardiovascular system: mechanisms and global health implications.Nature reviews. Cardiology · 2026Review
- Quercetin nanoparticles exhibit a potential therapeutic effect against the neurochemical changes and motor deficits in a rat model of Parkinson's disease.Scientific reports · 2026Article
- Effects of serotonin transporters on myocardial cell injury during ischemia/reperfusion in rats.The journal of physiological sciences : JPS · 2026Article
- Compartment-Specific Mitochondrial Proteomic Alterations in Rat Hippocampus Following Chronic Social Isolation Stress.International journal of molecular sciences · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- Potential molecular targets on which methylene blue acts to promote its effects on cardiac electrophysiology, myocardial injury, and oxidative stress in spontaneously hypertensive rats submitted to cardiac ischemia and reperfusion.Acta cirurgica brasileira · 2026Article
- Mitochondrial Dynamics in Aging Heart.Biomedicines · 2025Review
- The highs and lows of monoamine oxidase as molecular target in cancer: an updated review.Molecular and cellular biochemistry · 2025Review
- Inhibition of monoamine oxidases and neuroprotective effects: chalcones vs. chromones.Molecular diversity · 2025Article
- Comparison of the proteomic landscape in experimental ischemia reperfusion with versus without ischemic preconditioning.Scientific reports · 2025Article
- Serotonin signaling to regulate energy metabolism: a gut microbiota perspective.Life metabolism · 2025Review
- Elucidating the antioxidant potential of some flavanones as MAO-B inhibitors through DAM, in silico molecular docking and computational analysis.Plant molecular biology · 2025Article
- Measurement of Mitochondrial ROS Formation.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.Current cardiology reviews · 2025Review
- Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.Physiological research · 2024Review
- Synthesis of 1,2,4-Oxadiazin-5(6Molecules (Basel, Switzerland) · 2024Article
- Monoamine Oxidase Contributes to Valvular Oxidative Stress: A Prospective Observational Pilot Study in Patients with Severe Mitral Regurgitation.International journal of molecular sciences · 2024Observational
- Article
- Ameliorative effects of mesenchymal stromal cells on senescence associated phenotypes in naturally aged rats.Journal of translational medicine · 2024Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Oxidative stress can be generated at several sites within the mitochondria. Among these, monoamine oxidase (MAO) has been described as a prominent source. MAOs are mitochondrial flavoenzymes responsible for the oxidative deamination of catecholamines, serotonin and biogenic amines, and during this process they generate H2O2 and aldehyde intermediates. The role of MAO in cardiovascular pathophysiology has only recently gathered some attention since it has been demonstrated that both H2O2 and aldehydes may target mitochondrial function and consequently affect function and viability of the myocardium. In the present review, we will discuss the role of MAO in catecholamine and serotonin clearance and cycling in relation to cardiac structure and function. The relevant contribution of each MAO isoform (MAO-A or -B) will be discussed in relation to mitochondrial dysfunction and myocardial injury. Finally, we will examine both beneficial effects of their pharmacological or genetic inhibition along with potential adverse effects observed at baseline in MAO knockout mice, as well as the deleterious effects following their over-expression specifically at cardiomyocyte level. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".
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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.