ArticleFrontiers in physiology2017
Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning.
Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
- Article
- Trajectories of cardiovascular ageing-from molecular mechanisms to clinical implementation.Cardiovascular research · 2025Review
- Distribution of the p66Shc Adaptor Protein Among Mitochondrial and Mitochondria-Associated Membranes Fractions in Normal and Oxidative Stress Conditions.International journal of molecular sciences · 2024Article
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Deletion but Not Inhibition of Extracellular PCSK9 Reduces Infarct Sizes Ex Vivo but Not In Vivo.International journal of molecular sciences · 2022Article
- p66Shc signaling does not contribute to tubular damage induced by renal ischemia-reperfusion injury in rat.Biochemical and biophysical research communications · 2022Article
- Mechanism Involved in Acute Liver Injury Induced by Intestinal Ischemia-Reperfusion.Frontiers in pharmacology · 2022Review
- Mitochondria Isolated from Hearts Subjected to Ischemia/Reperfusion Benefit from Adenine Nucleotide Translocase 1 Overexpression.Membranes · 2021Article
- Lack of Contribution of p66shc to Pressure Overload-Induced Right Heart Hypertrophy.International journal of molecular sciences · 2020Article
- Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension.Redox biology · 2020Article
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
- The p66shc-mediated Regulation of Hepatocyte Senescence Influences Hepatic Steatosis in Nonalcoholic Fatty Liver Disease.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Mitochondrial dysfunction and oxidative stress in heart disease.Experimental & molecular medicine · 2019Review
- Mitochondria in Cardiac Postconditioning.Frontiers in physiology · 2018Review
- Baicalin Suppresses Hypoxia-Reoxygenation-Induced Arterial Endothelial Cell Apoptosis via Suppressing PKCδ/p53 Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whereas high amounts of reactive oxygen species (ROS) contribute to cardiac damage following ischemia and reperfusion (IR), low amounts function as trigger molecules in the cardioprotection by ischemic preconditioning (IPC). The mitochondrial translocation and contribution of the hydrogen peroxide-generating protein p66shc in the cardioprotection by IPC is unclear yet. In the present study, we investigated the mitochondrial translocation of p66shc, addressed the impact of p66shc on ROS formation after IR, and characterized the role of p66shc in IR injury
Indexed as
Identifiers
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.