ArticleBasic research in cardiology2023
Recent advances on the role of monoamine oxidases in cardiac pathophysiology.
Article in Basic research in cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.Basic research in cardiology · 2026Article
- Synthesis of 1,2,4-Oxadiazole Sulfonamide Derivatives and Their Biological Investigation as Monoamine Oxidase Inhibitors.Molecules (Basel, Switzerland) · 2026Article
- Therapeutic potential of CMPP, a novel maleimide derivative, in a reserpine-induced mouse model of pain-depression dyad.Biochemistry and biophysics reports · 2026Article
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- A Renal Clearable Probe for In Vivo Monoamine Oxidase (MAO) Detection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- Review
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- From mitochondrial zonation to immune dysregulation: a mechanistic axis in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- Metabolic Predictors of CAD: Focus on Cystine, Methionine, Proline, and Threonine Circulating Levels-Exploratory Pilot Study.Journal of clinical medicine · 2025Article
- 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
- Early-Stage Alcoholic Cardiomyopathy Highlighted by Metabolic Remodeling, Oxidative Stress, and Cardiac Myosin Dysfunction in Male Rats.International journal of molecular sciences · 2025Article
- Empagliflozin and dapagliflozin decreased atrial monoamine oxidase expression and alleviated oxidative stress in overweight non-diabetic cardiac patients.Molecular and cellular biochemistry · 2025Article
- Mechanisms of postischemic cardiac death and protection following myocardial injury.The Journal of clinical investigation · 2025Review
- Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.Physiological research · 2024Review
- Monoamine Oxidase Contributes to Valvular Oxidative Stress: A Prospective Observational Pilot Study in Patients with Severe Mitral Regurgitation.International journal of molecular sciences · 2024Observational
- Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection.Basic research in cardiology · 2024Review
- Comparison of the stage-dependent mitochondrial changes in response to pressure overload between the diseased right and left ventricle in the rat.Basic research in cardiology · 2024Article
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3 authors at 1 institution in 1 country.
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Abstract
Numerous physiological and pathological roles have been attributed to the formation of mitochondrial reactive oxygen species (ROS). However, the individual contribution of different mitochondrial processes independently of bioenergetics remains elusive and clinical treatments unavailable. A notable exception to this complexity is found in the case of monoamine oxidases (MAOs). Unlike other ROS-producing enzymes, especially within mitochondria, MAOs possess a distinct combination of defined molecular structure, substrate specificity, and clinically accessible inhibitors. Another significant aspect of MAO activity is the simultaneous generation of hydrogen peroxide alongside highly reactive aldehydes and ammonia. These three products synergistically impair mitochondrial function at various levels, ultimately jeopardizing cellular metabolic integrity and viability. This pathological condition arises from exacerbated MAO activity, observed in many cardiovascular diseases, thus justifying the exploration of MAO inhibitors as effective cardioprotective strategy. In this context, we not only summarize the deleterious roles of MAOs in cardiac pathologies and the positive effects resulting from genetic or pharmacological MAO inhibition, but also discuss recent findings that expand our understanding on the role of MAO in gene expression and cardiac development.
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