ReviewCardiovascular research2023
Mitochondrial calcium and reactive oxygen species in cardiovascular disease.
Review in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 88 citations in OpenAlex.
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- CYP2D6 as an Emerging Endogenous Oxidative Stress Modulator in Cardiovascular Disease: Genetic, Pharmacological, and Redox Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Oxidation-derived metabolites sustain the antioxidant network of quercetin.Journal of computer-aided molecular design · 2026Article
- Cardiotoxicity of Targeted Therapies in Hematologic Malignancies: From Molecular Mechanisms to Clinical Management.Current treatment options in oncology · 2026Review
- Sublethal stress from polypharmacy modulates scavenging function and fenestrations in mouse liver sinusoidal endothelial cells.The Journal of pharmacology and experimental therapeutics · 2026Article
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Acute Hypotensive Effects of 2-Acetylfuran and 5-Methylfurfural and Their Impact on Liver Mitochondrial Bioenergetics.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Proteomic signatures of mitochondrial dysfunction associated with atrial fibrillation in goats.Scientific reports · 2026Article
- Mitochondrial calcium uptake drives organelle remodeling to promote inflammasome-dependent cytokine release.Cell death and differentiation · 2026Article
- Local calcium dynamics and signalling in cardiomyocytes.Nature reviews. Cardiology · 2026Review
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- ROS-Mediated Cardiomyocyte Proliferation and Myocardial Regeneration: Mechanisms and Targeted Strategies for Ischemic Heart Disease.Journal of cardiovascular development and disease · 2026Review
- Molecular and Cellular Determinants of Human Iron Overload Cardiomyopathy.bioRxiv : the preprint server for biology · 2026Article
- The Landscape of SERCA2 in Cardiovascular Diseases: Expression Regulation, Therapeutic Applications, and Emerging Roles.Biomolecules · 2026Review
- Role and mechanisms of vascular smooth muscle cell phenotypic transition in diabetic macrovascular complications.Biological research · 2026Review
- Neutrophil immunometabolism in ACLF and sepsis: mechanisms, dysfunction, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Mitochondrial dysfunction in diabetic cardiomyopathy: a review of pathogenic mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- PCSK9 inhibition alleviates sepsis-induced myocardial dysfunction by facilitating PINK1/parkin-associated mitophagy.Frontiers in pharmacology · 2026Article
1 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 1 institution in 1 country.
Funding
Abstract
Cardiomyocytes are one of the most mitochondria-rich cell types in the body, with ∼30-40% of the cell volume being composed of mitochondria. Mitochondria are well established as the primary site of adenosine triphosphate (ATP) generation in a beating cardiomyocyte, generating up to 90% of its ATP. Mitochondria have many functions in the cell, which could contribute to susceptibility to and development of cardiovascular disease (CVD). Mitochondria are key players in cell metabolism, ATP production, reactive oxygen species (ROS) production, and cell death. Mitochondrial calcium (Ca2+) plays a critical role in many of these pathways, and thus the dynamics of mitochondrial Ca2+ are important in regulating mitochondrial processes. Alterations in these varied and in many cases interrelated functions play an important role in CVD. This review will focus on the interrelationship of mitochondrial energetics, Ca2+, and ROS and their roles in CVD. Recent insights into the regulation and dysregulation of these pathways have led to some novel therapeutic approaches.
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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.