The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury
Open accessAbstract
Background— Serotonin (5-hydroxytryptamine [5-HT]), released by activated platelets during cardiac ischemia, is metabolized by the mitochondrial enzyme monoamine oxidase A (MAO-A). Because hydrogen peroxide is one of the byproducts of 5-HT degradation by MAO-A, we investigated the potential role of reactive oxygen species generated by MAOs in 5-HT-dependent cardiomyocyte death and post-ischemia-reperfusion cardiac damage. Methods and Results— Treatment of isolated adult rat cardiomyocytes with 5-HT induced intracellular oxidative stress and cell apoptosis. The apoptotic cascade triggered by 5-HT involves release of cytochrome c, upregulation of proapoptotic Bax protein, and downregulation of antiapoptotic Bcl-2 protein. These effects were prevented by inhibition of amine transporter or MAO, antioxidants, or iron chelation. In contrast, cardiomyocyte apoptosis was only slightly affected by the 5-HT 2B receptor antagonist SB 206553. In vivo, inhibition of MAO-A largely reduced myocardial ultrastructural damage induced by 30 minutes of ischemia followed by 60 minutes of reperfusion in the rat heart. Cardioprotective effects of MAO inhibitors were associated with the prevention of postischemic oxidative stress, neutrophil accumulation, and mitochondrial-dependent cell death and were not reverted by SB 206553. Administration of MAO-A inhibitors during ischemia was still effective in preventing cardiac damage. Conclusions— Our results supply the first direct evidence that oxidative stress induced by MAO is responsible for receptor-independent apoptotic effects of 5-HT in cardiomyocytes and postischemic myocardial injury. These findings provide new insight into the mechanisms of 5-HT action in the heart and may constitute the basis for novel therapies.
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Cites
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Self-citationOxidative stress-elicited myocardial apoptosis during reperfusion
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Cited by
Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
Zorov, D. B., Juhaszova, M., & Sollott, S. J. (2014) · Physiological Reviews · doi:10.1152/physrev.00026.2013 · Cited by 5,383
Mitochondrial dysfunction and oxidative stress in heart disease
Peoples, J. N., Saraf, A., Ghazal, N., Pham, T. T., & Kwong, J. Q. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0355-7 · Cited by 950
Tanshinone IIA protects cardiac myocytes against oxidative stress-triggered damage and apoptosis
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Self-citationOxidative stress in early stage Bipolar Disorder and the association with response to lithium
de Sousa, R. T., Zarate, C. A., Zanetti, M. V., Costa, A. C., Talib, L. L., Gattaz, W. F., & Machado-Vieira, R. (2014) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2013.11.011 · Cited by 169
Metadata
- Authors
- Bianchi, P., Kunduzova, O., Masini, E., Cambon, C., Bani, D., Raimondi, L., Seguelas, M.-H., Nistri, S., Colucci, W., Leducq, N., & Parini, A.
- Venue
- Circulation
- Published
- 2005-11-22
- Volume
- 112
- Issue
- 21
- Pages
- 3297-3305
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2138567940
- Cited by
- 264
- References
- 26
- FWCI
- 3.85
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury. https://app.cochat.ai/papers/10.1161/circulationaha.104.528133
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- Bianchi, P., Kunduzova, O., Masini, E., Cambon, C., Bani, D., Raimondi, L., Seguelas, M.-H., Nistri, S., Colucci, W., Leducq, N., & Parini, A. (2005). Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury. Circulation. https://doi.org/10.1161/circulationaha.104.528133
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
