ReviewAntioxidants & redox signaling2015
Mitochondrial dynamics in diabetic cardiomyopathy.
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 75 papers.
What it found
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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.
The trial behind it
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
75 citing papers in PubMed, 125 citations in OpenAlex.
- Bariatric surgery may alleviate MASLD by restoring mitochondria-lipid droplet structural and functional integrity through suppression of the Mitochondrial Fission Factor-Perilipin 5 axis.Molecular biomedicine · 2026Article
- Reversing diastolic dysfunction in diabetes: a mitochondrial quality control-centric pharmacological approach.Acta diabetologica · 2026Review
- ATP6V0D2 Promotes Atherosclerosis-Associated Vascular Smooth Muscle Cell Dysfunction by Modulating Ferroptosis-Related Signaling.The journal of gene medicine · 2026Article
- Mitochondrial Dynamics in Diabetes Mellitus and Its Complications: Mechanisms, Pathological Roles, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Article
- GULP1 protects against diabetic cardiomyopathy through IKIP/NF-κB-dependent improvement of mitochondrial function.Cardiovascular diabetology · 2026Article
- A TFAP4-UBC9-SUMO1 axis orchestrates pathological mitochondrial hyperfission in diabetic complications.Acta diabetologica · 2026Article
- PCSK9 Inhibitor Alirocumab Improves Diabetic Cardiomyopathy Through the ERK/p38 MAPK Signaling Pathway.International journal of molecular sciences · 2026Article
- Integrative insights into fatty acid metabolism in diabetic cardiomyopathy: From molecular mechanisms to therapeutic strategies.iScience · 2026Review
- Imbalance in MICOS Proteins in Rat Liver Mitochondria in an Induced Hyperthyroidism Model.Cells · 2025Article
- SIRT4 Protects Müller Glial Cells Against Apoptosis by Mediating Mitochondrial Dynamics and Oxidative Stress.Molecular neurobiology · 2025Article
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Syntaxin 17 Translocation Mediated Mitophagy Switching Drives Hyperglycemia-Induced Vascular Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025Review
- High glucose affects the cardiac function of diabetic Akita mice by inhibiting cardiac ATP synthase beta subunit.International journal of cardiology. Cardiovascular risk and prevention · 2025Article
- The cardiac response of the goldfish Carassius auratus to environmental hypoxia: from hemodynamics to mitochondria.Fish physiology and biochemistry · 2025Article
- Molecular Pathways in Diabetic Cardiomyopathy and the Role of Anti-hyperglycemic Drugs Beyond Their Glucose Lowering Effect.Journal of lipid and atherosclerosis · 2025Review
- ZIP7 contributes to the pathogenesis of diabetic cardiomyopathy by suppressing mitophagy in mouse hearts.Cardiovascular diabetology · 2024Article
- Therapeutic potential of finerenone for diabetic cardiomyopathy: focus on the mechanisms.Diabetology & metabolic syndrome · 2024Review
- The application of extracorporeal shock wave therapy on stem cells therapy to treat various diseases.Stem cell research & therapy · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
significanceCardiac function is energetically demanding, reliant on efficient well-coupled mitochondria to generate adenosine triphosphate and fulfill the cardiac demand. Predictably then, mitochondrial dysfunction is associated with cardiac pathologies, often related to metabolic disease, most commonly diabetes. Diabetic cardiomyopathy (DCM), characterized by decreased left ventricular function, arises independently of coronary artery disease and atherosclerosis. Dysregulation of Ca(2+) handling, metabolic changes, and oxidative stress are observed in DCM, abnormalities reflected in alterations in mitochondrial energetics. Cardiac tissue from DCM patients also presents with altered mitochondrial morphology, suggesting a possible role of mitochondrial dynamics in its pathological progression. RECENT ADVANCES: Abnormal mitochondrial morphology is associated with pathologies across diverse tissues, suggesting that this highly regulated process is essential for proper cell maintenance and physiological homeostasis. Highly structured cardiac myofibers were hypothesized to limit alterations in mitochondrial morphology; however, recent work has identified morphological changes in cardiac tissue, specifically in DCM. CRITICAL ISSUES: Mitochondrial dysfunction has been reported independently from observations of altered mitochondrial morphology in DCM. The temporal relationship and causative nature between functional and morphological changes of mitochondria in the establishment/progression of DCM is unclear. FUTURE DIRECTIONS: Altered mitochondrial energetics and morphology are not only causal for but also consequential to reactive oxygen species production, hence exacerbating oxidative damage through reciprocal amplification, which is integral to the progression of DCM. Therefore, targeting mitochondria for DCM will require better mechanistic characterization of morphological distortion and bioenergetic dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.