ReviewInternational journal of molecular sciences2025
Mitochondrial Dysfunction in Cardiovascular Diseases.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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
52 citing papers in PubMed.
- Targeting FOXO3 for the Management of Heart Failure: Current Evidence and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- From Retina to Vasculature: Oxidative Stress as a Common Mechanistic Link Between Age-Related Macular Degeneration and Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2026Review
- Immunomodulatory Nanozymes as Programmable Redox-Immune Set-Point Regulators.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- Cardiovascular Diseases: Exploring Epidemiology, Pathophysiology, Risk Factors, and Medicinal Plant-Based Therapies: A Narrative Review.Health science reports · 2026Article
- A Mechanism-Centered Text-Mining Landscape of Mitochondrial Bioenergetics and Signaling in Disease Research.International journal of molecular sciences · 2026Review
- From Continuous-Flow Mechanical Circulatory Support to Heart Transplantation: Hemodynamic, Immunometabolic, and Body Composition Determinants of Rehabilitation Outcomes.Journal of clinical medicine · 2026Review
- Mitochondrial Dysfunction in Circulating Blood Cells and Biological Aging: A Review of Mechanisms and Evidence.Biomolecules · 2026Review
- Mitochondrial UQCRC2 as a Redox-Regulatory Node in Metabolic and Cardiometabolic Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- ALYREF stabilizes MZF1 via m5C modification to exacerbate cardiac remodeling and atrial fibrillation in heart failure.Cellular and molecular life sciences : CMLS · 2026Article
- The Bidens pilosa extract Jacein alleviates hypertension by restoring mitochondrial dynamic balance through modulating the FAM210A/OPA1 signaling pathway.Molecular and cellular biochemistry · 2026Article
- The role of mitochondrial dysfunction, oxidative stress, and gender in cardiac fibrosis and vascular remodeling in an induced aged rat model with possible mitigation by eugenol nano-emulsion.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Long-term temporal stability of circulating proteins in older adults.Nature communications · 2026Article
- Article
- Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis.Archives of toxicology · 2026Review
- Ginkgetin Alleviates Doxorubicin-Induced Heart Failure by Regulating Mitochondrial Dysfunction Through the AMPK/Sirt1/NF-κB Signaling Pathway.Balkan medical journal · 2026Article
- MicroRNAs in Cardiovascular Diseases: Molecular Networks of Cellular Homeostasis, Inflammation, and Pathological Remodeling.International journal of molecular sciences · 2026Review
- Next-Generation Metabolic Reprogramming in iPSC-Derived Cardiomyocytes: CRISPR-EV Synergy for Precision Cardiac Regeneration.Biomolecules · 2026Review
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- Review
- From Exposure to Atherosclerosis: Mechanistic Insights into Phthalate-Driven Ischemic Heart Disease and Prevention Strategies.Life (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Mitochondrial dysfunction is increasingly recognized as a central contributor to the pathogenesis of cardiovascular diseases (CVDs), including heart failure, ischemic heart disease, hypertension, and cardiomyopathy. Mitochondria, known as the powerhouses of the cell, play a vital role in maintaining cardiac energy homeostasis, regulating reactive oxygen species (ROS) production and controlling cell death pathways. Dysregulated mitochondrial function results in impaired adenosine triphosphate (ATP) production, excessive ROS generation, and activation of apoptotic and necrotic pathways, collectively driving the progression of CVDs. This review provides a detailed examination of the molecular mechanisms underlying mitochondrial dysfunction in CVDs, including mutations in mitochondrial DNA (mtDNA), defects in oxidative phosphorylation (OXPHOS), and alterations in mitochondrial dynamics (fusion, fission, and mitophagy). Additionally, the role of mitochondrial dysfunction in specific cardiovascular conditions is explored, highlighting its impact on endothelial dysfunction, myocardial remodeling, and arrhythmias. Emerging therapeutic strategies targeting mitochondrial dysfunction, such as mitochondrial antioxidants, metabolic modulators, and gene therapy, are also discussed. By synthesizing recent advances in mitochondrial biology and cardiovascular research, this review aims to enhance understanding of the role of mitochondria in CVDs and identify potential therapeutic targets to improve cardiovascular outcomes.
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What OpenQuestion holds
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.