Journal article
Not 'Inactive' After All: Cardiotoxic Mechanisms of Catecholamine Metabolism by Monoamine Oxidase
Cardiovascular toxicology, Vol.25, pp.1202-1221
06/10/2025
DOI: 10.1007/s12012-025-10021-7
PMCID: PMC12267328
PMID: 40495031
Appears in UI Libraries Support Open Access
Abstract
Monoamine oxidase (MAO) helps regulate catecholaminergic signaling via metabolism of neurotransmitters epinephrine, norepinephrine, and dopamine—in turn producing the metabolites hydrogen peroxide (H2O2), ammonia (NH4+), and corresponding catecholaldehydes. While MAO has been a key facet of neuroscience and mood disorder research for > 60 years, MAO-generated metabolites have been largely overlooked until recently when reports have begun to illustrate the reactivity of these metabolites and their pathogenic contributions to disease (e.g., inflammation, fibrosis, cell death). These findings have extended MAO’s biological relevance beyond the brain and, most notably, to the heart, where a large and growing body of literature clearly indicates a pathophysiologic role for MAO-mediated catecholamine metabolism in heart disease. Herein, we discuss the evidence connecting MAO to various cardiac injuries and disorders, as well as describe the known cardiotoxicity associated with MAO’s reactive metabolites, specifically in connection to cardiac pathophysiology. Potential therapeutic strategies for targeting MAO and its metabolites to prevent and treat heart disease are also discussed, and important knowledge gaps highlighted.
Details
- Title: Subtitle
- Not 'Inactive' After All: Cardiotoxic Mechanisms of Catecholamine Metabolism by Monoamine Oxidase
- Creators
- Rachel M Crawford - Department of Pharmaceutical Sciences & Experimental Therapeutics, College of Pharmacy, University of Iowa, 180 S Grand Avenue, Iowa City, IA, 52242, USAEthan J Anderson - Abboud Cardiovascular Research Center, University of Iowa, Iowa City, IA, 52242, USA. ethan-anderson@uiowa.edu
- Resource Type
- Journal article
- Publication Details
- Cardiovascular toxicology, Vol.25, pp.1202-1221
- DOI
- 10.1007/s12012-025-10021-7
- PMID
- 40495031
- PMCID
- PMC12267328
- NLM abbreviation
- Cardiovasc Toxicol
- ISSN
- 1559-0259
- eISSN
- 1559-0259
- Publisher
- Springer Nature
- Grant note
- R01HL167087 / NHLBI NIH HHS 20SFRN35200003 / American Heart Association
- Language
- English
- Date published
- 06/10/2025
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Fraternal Order of Eagles Diabetes Research Center
- Record Identifier
- 9984829883102771
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