ReviewExperimental & molecular medicine2019
Mitochondrial dysfunction and oxidative stress in heart disease.
Review in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 553 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
553 citing papers in PubMed, 3 syntheses or guidelines pooled it, 872 citations in OpenAlex.
- Mitochondrial-inflammation crosstalk in major depressive disorder: molecular mechanisms and therapeutic implications.Molecular psychiatry · 2026Pooled it
- Cardioprotection Through Mitochondrial Modulation: A Systematic Review of Pharmacological Interventions in Animal Models of I/R Injury.Cardiovascular drugs and therapy · 2026Pooled it
- Tumor Extracellular Vesicles Aggravate Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Pooled it
- Eight weeks of MitoQ supplementation does not alter kidney function or urinary kidney injury biomarkers in middle-aged and older adults.American journal of physiology. Renal physiology · 2026Trial
- MitoQ supplementation does not impact redox responses to acute exercise in skeletal muscle of older individuals.Redox biology · 2025Trial
- Imbalance of mitochondria and abnormalities in lipid metabolism in Diabetic Tubulopathy.Annals of medicine · 2026Review
- Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated deubiquitination of PRDX2.International journal of molecular medicine · 2026Article
- Sepsis-associated endothelial dysfunction: clinical phenotypes, biomarkers, bedside evidence, and translational implications.The Journal of clinical investigation · 2026Review
- Association between overall dietary antioxidant capacity and lung cancer risk: findings from two observational studies.European journal of epidemiology · 2026Article
- A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial dysfunction and oxidative stress in OSAHS and associated comorbidities: Mechanism and potential targeted therapeutic strategies.Redox biology · 2026Review
- Article
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Organelle network dysfunction in primary cardiomyopathy: An integrated perspective on pathogenesis and therapeutics.Journal of molecular and cellular cardiology plus · 2026Review
- Echoes in the powerhouse: mito-lncRNAs contribution to cardiac function and disease.Acta pharmacologica Sinica · 2026Review
- CHK1 activates mitophagy to attenuate cardiac aging via inhibiting AHSA1-ubiquitination.Redox biology · 2026Article
- Review
- BCKDK protects against obesity-induced cardiac remodelling and dysfunction by alleviating mitochondrial oxidative stress and ROS-driven MAPK signalling.Redox biology · 2026Article
- Ginsenoside Rg2 Targeting PDHE1 α to Improve High Glucose-Induced Hippocampal Neuronal Damage Based on CETSA Experiment.Chinese journal of integrative medicine · 2026Article
493 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated process driving oxidative stress and disease pathology, contemporary studies reveal that ROS also facilitate normal physiology. Mitochondria are especially abundant in cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Moreover, there is growing appreciation that medical therapies designed to mediate mitochondrial ROS production can be important strategies to ameliorate cardiac disease. In this review, we highlight evidence from animal models that illustrates the strong connections between mitochondrial ROS and cardiac disease, discuss advancements in the development of mitochondria-targeted antioxidant therapies, and identify challenges faced in bringing such therapies into the clinic.
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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.