ReviewAntioxidants & redox signaling2015
Protective mechanisms of mitochondria and heart function in diabetes.
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 40 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Progress in the treatment of diabetic cardiomyopathy, a systematic review.Pharmacology research & perspectives · 2024Pooled it
- Effects of moderate-intensity continuous training on cardiac mitochondrial bioenergetics, oxidative balance, and mitochondrial dynamic in juvenile overnourished rats.Molecular and cellular biochemistry · 2026Article
- MOTS-c preserves mitochondrial subpopulation bioenergetics and genome integrity to attenuate cardiac ischemia reperfusion injury.Molecular biology reports · 2026Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.The Journal of clinical investigation · 2026Article
- Iron Deficiency as a Modifiable Risk Factor in Heart Failure: Evidence and Recommendations.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026Review
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Understanding cardiovascular aging as a disorder of mitochondrial network.The journal of cardiovascular aging · 2026Article
- Dihydroorotate Dehydrogenase as a Modulator of Ferroptosis in Myocardial Ischemia-reperfusion Injury.Current molecular medicine · 2026Article
- The crosstalk between immune activation and metabolism in heart failure. A scientific statement of the Heart Failure Association of the ESC.European journal of heart failure · 2025Review
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- Macrod1 suppresses diabetic cardiomyopathy via regulating PARP1-NADActa pharmacologica Sinica · 2024Article
- Article
- Cardiovascular protection of YiyiFuzi powder and the potential mechanisms through modulating mitochondria-endoplasmic reticulum interactions.Frontiers in pharmacology · 2024Review
- Novel insights into the role of mitochondria in diabetic cardiomyopathy: molecular mechanisms and potential treatments.Cell stress & chaperones · 2023Review
- Mitochondrial and Proteasome Dysfunction Occurs in the Hearts of Mice Treated with Triazine Herbicide Prometryn.International journal of molecular sciences · 2023Article
- Prognostic impact of diabetes in chronic and acute heart failure.Heart failure reviews · 2023Review
- Changes in Cardiac Metabolism in Prediabetes.Biomolecules · 2021Review
- Mitochondrial health is enhanced in rats with higher vs. lower intrinsic exercise capacity and extended lifespan.NPJ aging and mechanisms of disease · 2021Article
- Nutrition, Bioenergetics, and Metabolic Syndrome.Nutrients · 2020Review
- Redox Imbalances in Ageing and Metabolic Alterations: Implications in Cancer and Cardiac Diseases. An Overview from the Working Group of Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology (SIC).Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
significanceThe heart depends on continuous mitochondrial ATP supply and maintained redox balance to properly develop force, particularly under increased workload. During diabetes, however, myocardial energetic-redox balance is perturbed, contributing to the systolic and diastolic dysfunction known as diabetic cardiomyopathy (DC). CRITICAL ISSUES: How these energetic and redox alterations intertwine to influence the DC progression is still poorly understood. Excessive bioavailability of both glucose and fatty acids (FAs) play a central role, leading, among other effects, to mitochondrial dysfunction. However, where and how this nutrient excess affects mitochondrial and cytoplasmic energetic/redox crossroads remains to be defined in greater detail. RECENT ADVANCES: We review how high glucose alters cellular redox balance and affects mitochondrial DNA. Next, we address how lipid excess, either stored in lipid droplets or utilized by mitochondria, affects performance in diabetic hearts by influencing cardiac energetic and redox assets. Finally, we examine how the reciprocal energetic/redox influence between mitochondrial and cytoplasmic compartments shapes myocardial mechanical activity during the course of DC, focusing especially on the glutathione and thioredoxin systems. FUTURE DIRECTIONS: Protecting mitochondria from losing their ability to generate energy, and to control their own reactive oxygen species emission is essential to prevent the onset and/or to slow down DC progression. We highlight mechanisms enforced by the diabetic heart to counteract glucose/FAs surplus-induced damage, such as lipid storage, enhanced mitochondria-lipid droplet interaction, and upregulation of key antioxidant enzymes. Learning more on the nature and location of mechanisms sheltering mitochondrial functions would certainly help in further optimizing therapies for human DC.
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