ReviewAntioxidants & redox signaling2015
Metabolic alterations induce oxidative stress in diabetic and failing hearts: different pathways, same outcome.
Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms, Current Treatment and Therapeutic Potential of Plant Antioxidants.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Tibial fracture surgery in elderly mice caused postoperative neurocognitive disorder via SOX2OT lncRNA in the hippocampus.Molecular brain · 2023Article
- Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- The Role of Mitochondria in Metabolic Syndrome-Associated Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
- Possible Synergistic Antidiabetic Effects of QuantifiedBiology · 2021Article
- Effects of Bergamot Polyphenols on Mitochondrial Dysfunction and Sarcoplasmic Reticulum Stress in Diabetic Cardiomyopathy.Nutrients · 2021Review
- Allisartan isoproxil attenuates oxidative stress and inflammation through the SIRT1/Nrf2/NF‑κB signalling pathway in diabetic cardiomyopathy rats.Molecular medicine reports · 2021Article
- Roles of HDAC3-orchestrated circadian clock gene oscillations in diabetic rats following myocardial ischaemia/reperfusion injury.Cell death & disease · 2021Article
- Inflammasome as an Effective Platform for Fibrosis Therapy.Journal of inflammation research · 2021Review
- Redox à la carte: Novel chemogenetic models of heart failure.British journal of pharmacology · 2020Review
- Diabetes Increases the Vulnerability of the Cardiac Mitochondrial Network to Criticality.Frontiers in physiology · 2020Article
- Mitochondrial ROS Formation in the Pathogenesis of Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2020Review
- Downregulation of TRAP1 aggravates injury of H9c2 cardiomyocytes in a hyperglycemic state.Experimental and therapeutic medicine · 2019Article
- Control and Regulation of Substrate Selection in Cytoplasmic and Mitochondrial Catabolic Networks. A Systems Biology Analysis.Frontiers in physiology · 2019Article
- Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling.Oxidative medicine and cellular longevity · 2019Article
- Astragaloside IV Attenuates Myocardial Ischemia-Reperfusion Injury from Oxidative Stress by Regulating Succinate, Lysophospholipid Metabolism, and ROS Scavenging System.Oxidative medicine and cellular longevity · 2019Article
- Metabolic Effects of Metformin in the Failing Heart.International journal of molecular sciences · 2018Review
- Effect of N-Acetylcysteine on Dyslipidemia and Carbohydrate Metabolism in STZ-Induced Diabetic Rats.International journal of vascular medicine · 2018Article
- Stress Coping Strategies in the Heart: An Integrated View.Frontiers in cardiovascular medicine · 2018Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
significanceSeveral authors have proposed a link between altered cardiac energy substrate metabolism and reactive oxygen species (ROS) generation. A cogent evidence of this association has been found in diabetic cardiomyopathy (dCM); however, experimental findings in animal models of heart failure (HF) and in human myocardium also seem to support the coexistence of the two alterations in HF. CRITICAL ISSUES: Two important questions remain open: whether pathological changes in metabolism play an important role in enhancing oxidative stress and whether there is a common pathway linking altered substrate utilization and activation of ROS-generating enzymes, independently of the underlying cardiac pathology. In this regard, the comparison between dCM and HF is intriguing, in that these pathological conditions display very different cardiac metabolic phenotypes. RECENT ADVANCES: Our literature review on this topic indicates that a vast body of knowledge is now available documenting the relationship between the metabolism of energy substrates and ROS generation in dCM. In some cases, biochemical mechanisms have been identified. On the other hand, only a few and relatively recent studies have explored this phenomenon in HF and their conclusions are not consistent. FUTURE DIRECTIONS: Better methods of investigation, especially in vivo, will be necessary to test whether the metabolic fate of certain substrates is causally linked to ROS production. If successful, these studies will place a new emphasis on the potential clinical relevance of metabolic modulators, which might indirectly mitigate cardiac oxidative stress in dCM, HF, and, possibly, in other pathological conditions.
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