ReviewMolecular neurobiology2017
P66
Review in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 40 citations in OpenAlex.
- HDACs and Their Inhibitors on Post-Translational Modifications: The Regulation of Cardiovascular Disease.Cells · 2025Review
- Emerging insights into the pathogenesis and therapeutic strategies for vascular endothelial injury-associated diseases: focus on mitochondrial dysfunction.Angiogenesis · 2024Review
- Oxidative stress and senescence in aging kidneys: the protective role of SIRT1.EXCLI journal · 2024Review
- CSE triggers ferroptosis via SIRT4-mediated GNPAT deacetylation in the pathogenesis of COPD.Respiratory research · 2023Article
- Allii Macrostemonis Bulbus: A Comprehensive Review of Ethnopharmacology, Phytochemistry and Pharmacology.Molecules (Basel, Switzerland) · 2023Review
- Targeting SIRT1 Rescues Age- and Obesity-Induced Microvascular Dysfunction in Ex Vivo Human Vessels.Circulation research · 2022Article
- The role of Sirtuin 1 in the pathophysiology of polycystic ovary syndrome.European journal of medical research · 2022Review
- Mitochondrial Dysfunction in Oxidative Stress-Mediated Intervertebral Disc Degeneration.Orthopaedic surgery · 2022Review
- Mechanisms and clinical implications of endothelium-dependent vasomotor dysfunction in coronary microvasculature.American journal of physiology. Heart and circulatory physiology · 2022Review
- Proteomic profiling of cisplatin-resistant and cisplatin-sensitive germ cell tumour cell lines using quantitative mass spectrometry.World journal of urology · 2022Article
- Sirtuin 2 Alleviates Chronic Neuropathic Pain by Suppressing Ferroptosis in Rats.Frontiers in pharmacology · 2022Article
- Human SHC-transforming protein 1 and its isoforms p66shc: A novel marker for prediabetes.Journal of diabetes investigation · 2021Article
- 20-HETE synthesis inhibition attenuates traumatic brain injury-induced mitochondrial dysfunction and neuronal apoptosis via the SIRT1/PGC-1α pathway: A translational study.Cell proliferation · 2021Article
- Oxidative Stress in Intestinal Ischemia-Reperfusion.Frontiers in medicine · 2021Review
- Low-density lipoprotein receptor (LDLR) regulates NLRP3-mediated neuronal pyroptosis following cerebral ischemia/reperfusion injury.Journal of neuroinflammation · 2020Article
- Endothelial dysfunction in neuroprogressive disorders-causes and suggested treatments.BMC medicine · 2020Review
- Suppression of p66Shc prevents hyperandrogenism-induced ovarian oxidative stress and fibrosis.Journal of translational medicine · 2020Article
- Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease.Nature reviews. Cardiology · 2020Review
- circ-PRKCB acts as a ceRNA to regulate p66Shc-mediated oxidative stress in intestinal ischemia/reperfusion.Theranostics · 2020Article
- Downregulation of p66Shc can reduce oxidative stress and apoptosis in oxidative stress model of marginal cells of stria vascularis in Sprague Dawley rats.Drug design, development and therapy · 2019Article
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 at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence shows that acute and chronic overproduction of reactive oxygen species (ROS) and increased oxidants under pathophysiologic circumstances are of vital importance in the development of cardio-cerebral vascular diseases (CCVDs). It has been revealed that the impact of ROS can be suppressed by sirtuin 1 (SIRT1), a member of the highly conserved nicotinamide adenine dinucleotide-dependent class III histone deacetylases through protecting endothelial cells from oxidative injury. Plenty of evidences indicate that p66Shc stimulates mitochondrial ROS generation through its oxidoreductase activity and plays a vital role in the pathophysiology of CCVDs. The link between SIRT and p66Shc, though not very clear yet, may be generally illustrated like this: SIRT1 negatively regulates the expression of p66Shc in transcriptional level. In this review, the authors aimed to discuss the link between the pathogenesis of CCVDs, the regulation of ROS, the interrelation between SIRT1 and p66Shc, and the protective effect of the proper regulation of p66Shc/SIRT1 on CCVDs. The imbalance between the elimination and production of ROS can lead to oxidative stress (OS). More and more evidence suggest that ROS pathological overproduction is closely connected to the genesis and growth of CCVDs. P66shc is a gene that controls ROS level, apoptosis induction, and lifespan. Lots of evidence also indicate a role for SIRT1 mediating OS responses through several ways including directly deacetylating some transcription factors that control anti-OS genes. SIRT1 downregulation can lead to a decreased deacetylation of p66shc gene promoter and can then result in p66shc transcription. SIRT1 binds to the promoter of p66Shc where it can deacetylate histone H3, which weakens the transcription and translation of p66shc.
Indexed as
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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.