ArticleOxidative medicine and cellular longevity2016
Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- Substrate-specific mitochondrial dysfunction and metabolomic profiles in type 2 diabetic rat hearts.Experimental physiology · 2026Article
- Mitochondrial respiration and hydrogen peroxide production rate in right atrial tissues from obese diabetic patients.Experimental physiology · 2026Article
- Assessing the interaction of the UCP system and fatty acids on epicardial adipose tissue mitochondrial respiration.European journal of clinical investigation · 2026Article
- Not 'Inactive' After All: Cardiotoxic Mechanisms of Catecholamine Metabolism by Monoamine Oxidase.Cardiovascular toxicology · 2025Review
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- Methylene blue reduces monoamine oxidase expression and oxidative stress in human cardiovascular adipose tissue.Molecular and cellular biochemistry · 2025Article
- Empagliflozin and dapagliflozin decreased atrial monoamine oxidase expression and alleviated oxidative stress in overweight non-diabetic cardiac patients.Molecular and cellular biochemistry · 2025Article
- Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.Physiological research · 2024Review
- Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms.Journal of molecular and cellular cardiology · 2024Review
- Multiplatform tear proteomic profiling reveals novel non-invasive biomarkers for diabetic retinopathy.Eye (London, England) · 2024Article
- Assessing the Relationship between Indexed Epicardial Adipose Tissue Thickness, Oxidative Stress in Adipocytes, and Coronary Artery Disease Complexity in Open-Heart Surgery Patients.Medicina (Kaunas, Lithuania) · 2024Article
- Novel Strategies in the Early Detection and Treatment of Endothelial Cell-Specific Mitochondrial Dysfunction in Coronary Artery Disease.Antioxidants (Basel, Switzerland) · 2023Review
- A Review ofMolecules (Basel, Switzerland) · 2023Review
- Review
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Redox Properties of 3-Iodothyronamine (T1AM) and 3-Iodothyroacetic Acid (TA1).International journal of molecular sciences · 2022Article
- Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress.International journal of molecular sciences · 2022Review
- Metformin alleviates monoamine oxidase-related vascular oxidative stress and endothelial dysfunction in rats with diet-induced obesity.Molecular and cellular biochemistry · 2021Article
- Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria-related oxidative stress is a pathomechanism causally linked to coronary heart disease (CHD) and diabetes mellitus (DM). Recently, mitochondrial monoamine oxidases (MAOs) have emerged as novel sources of oxidative stress in the cardiovascular system and experimental diabetes. The present study was purported to assess the mitochondrial impairment and the contribution of MAOs-related oxidative stress to the cardiovascular dysfunction in coronary patients with/without DM. Right atrial appendages were obtained from 75 patients randomized into 3 groups: (1) Control (CTRL), valvular patients without CHD; (2) CHD, patients with confirmed CHD; and (3) CHD-DM, patients with CHD and DM. Mitochondrial respiration was measured by high-resolution respirometry and MAOs expression was evaluated by RT-PCR and immunohistochemistry. Hydrogen peroxide (H2O2) emission was assessed by confocal microscopy and spectrophotometrically. The impairment of mitochondrial respiration was substrate-independent in CHD-DM group. MAOs expression was comparable among the groups, with the predominance of MAO-B isoform but no significant differences regarding oxidative stress were detected by either method. Incubation of atrial samples with MAOs inhibitors significantly reduced the H2O2 in all groups. In conclusion, abnormal mitochondrial respiration occurs in CHD and is more severe in DM and MAOs contribute to oxidative stress in human diseased hearts with/without DM.
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