ReviewHeart failure reviews2007
Mitochondria and cardioprotection.
Review in Heart failure reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed.
- Circulating Mitochondrial DNA Aggravates Post-Ischemic Functional and Metabolic Recovery in an Isolated Rat Heart Model of Donation After Circulatory Death.International journal of molecular sciences · 2026Article
- The Noncanonical Wnt5a-CaJournal of cellular and molecular medicine · 2025Article
- Calcium signaling from sarcoplasmic reticulum and mitochondria contact sites in acute myocardial infarction.Journal of translational medicine · 2024Review
- Nanoparticle-Based Interventions for Liver Transplantation.International journal of molecular sciences · 2023Review
- Article
- Hypothermia for Cardioprotection in Patients with St-Elevation Myocardial Infarction: Do Not Give It the Cold Shoulder Yet!Journal of clinical medicine · 2022Review
- Network-Assisted Systems Biology Analysis of the Mitochondrial Proteome in a Pre-Clinical Model of Ischemia, Revascularization and Post-Conditioning.International journal of molecular sciences · 2022Article
- Mitochondrial DNA Release Contributes to Intestinal Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2022Review
- Combating Ischemia-Reperfusion Injury with Micronutrients and Natural Compounds during Solid Organ Transplantation: Data of Clinical Trials and Lessons of Preclinical Findings.International journal of molecular sciences · 2021Review
- [Perioperative cardioprotection - From bench to bedside : Current experimental evidence and possible reasons for the limited translation into the clinical setting].Der Anaesthesist · 2021Review
- Combination of Cyclosporine A and Levosimendan Induces Cardioprotection under Acute Hyperglycemia.International journal of molecular sciences · 2021Article
- Cardioprotective Properties of Mannitol-Involvement of Mitochondrial Potassium Channels.International journal of molecular sciences · 2021Article
- Roles of LncRNAs in Regulating Mitochondrial Dysfunction in Septic Cardiomyopathy.Frontiers in immunology · 2021Review
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
- MKP-1 Overexpression Reduces Postischemic Myocardial Damage through Attenuation of ER Stress and Mitochondrial Damage.Oxidative medicine and cellular longevity · 2021Article
- Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.International journal of molecular sciences · 2020Review
- Intracellular Chloride Channels: Novel Biomarkers in Diseases.Frontiers in physiology · 2020Review
- Inhibition of chymotrypsin-like activity of the proteasome by ixazomib prevents mitochondrial dysfunction during myocardial ischemia.PloS one · 2020Article
- Adenosine AJournal of cellular physiology · 2019Article
- Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major factors linking mitochondrial dysfunction with myocardial injury are analyzed along with protective mechanisms elicited by endogenous processes and pharmacological treatments. In particular, a reduced rate of ATP hydrolysis and a slight increase in ROS formation appear to represent the prevailing components of self-defense mechanisms, especially in the case of ischemic preconditioning. These protective processes are activated by signaling pathways, which converge on mitochondria activating the mitochondrial K(ATP) channels and/or inhibiting the mitochondrial permeability transition pore. These pathways can also be stimulated by pharmacological treatments. Another major goal for cardioprotection is decreasing the burst in mitochondrial ROS formation that characterizes post-ischemic reperfusion. Finally, mitochondrial targets for therapeutic intervention may include the switch of substrate being utilized, because inhibition of fatty acid oxidation is associated with cardioprotective effects.
Indexed as
Identifiers
17516167What 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.