ReviewBritish journal of pharmacology2017
New aspects of p66Shc in ischaemia reperfusion injury and other cardiovascular diseases.
Review in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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
47 citing papers in PubMed, 65 citations in OpenAlex.
- Tranexamic acid inhibits mitochondrial DNA release and reduces inflammatory response in an in vitro model of OGD/R-induced Caco-2 cell injury.BMC pharmacology & toxicology · 2026Article
- Tyrosine 48 Phosphorylation of CytochromeBiomolecules · 2026Article
- Mitochondrial Reactive Oxygen Species: A Unifying Mechanism in Long COVID and Spike Protein-Associated Injury: A Narrative Review.Biomolecules · 2025Review
- Oxidative Stress in the Pathophysiology of Chronic Venous Disease: An Overview.Antioxidants (Basel, Switzerland) · 2025Review
- Prevention of hypertension-induced renal vascular dysfunction through a p66Shc-targeted mechanism.American journal of physiology. Renal physiology · 2025Article
- Cardiac Tyrosine 97 Phosphorylation of CytochromeInternational journal of molecular sciences · 2025Article
- Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia-reperfusion injury.Clinical and translational medicine · 2025Review
- The Role of the Redox Enzyme p66Shc in Biological Aging of the Lung.Aging and disease · 2024Article
- Phosphorylations and Acetylations of CytochromeCells · 2024Review
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- Salvianolic Acid A Protects against Acetaminophen-Induced Hepatotoxicity via Regulation of the miR-485-3p/SIRT1 Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- USP15 regulates p66Shc stability associated with Drp1 activation in liver ischemia/reperfusion.Cell death & disease · 2022Article
- p66Shc in Cardiovascular Pathology.Cells · 2022Review
- Genetic deletion of p66shc and/or cyclophilin D results in decreased pulmonary vascular tone.Cardiovascular research · 2022Article
- The Role of Mitochondria in Metabolic Syndrome-Associated Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial DNA Release Contributes to Intestinal Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2022Review
- Maintaining Effective Beta Cell Function in the Face of Metabolic Syndrome-Associated Glucolipotoxicity-Nutraceutical Options.Healthcare (Basel, Switzerland) · 2021Review
- Piperazine ferulate attenuates high glucose‑induced mesangial cell injury via the regulation of p66Molecular medicine reports · 2021Article
- Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although reactive oxygen species (ROS) act as crucial factors in the onset and progression of a wide array of diseases, they are also involved in numerous signalling pathways related to cell metabolism, growth and survival. ROS are produced at various cellular sites, and it is generally agreed that mitochondria generate the largest amount, especially those in cardiomyocytes. However, the identification of the most relevant sites within mitochondria, the interaction among the various sources, and the events responsible for the increase in ROS formation under pathological conditions are still highly debated, and far from being clarified. Here, we review the information linking the adaptor protein p66Shc with cardiac injury induced by ischaemia and reperfusion (I/R), including the contribution of risk factors, such as metabolic syndrome and ageing. In response to several stimuli, p66Shc migrates into mitochondria where it catalyses electron transfer from cytochrome c to oxygen resulting in hydrogen peroxide formation. Deletion of p66Shc has been shown to reduce I/R injury as well as vascular abnormalities associated with diabetes and ageing. However, p66Shc-induced ROS formation is also involved in insulin signalling and might contribute to self-endogenous defenses against mild I/R injury. In addition to its role in physiological and pathological conditions, we discuss compounds and conditions that can modulate the expression and activity of p66Shc. LINKED ARTICLES: This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.
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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.