ReviewAntioxidants & redox signaling2011
Signal transducers and activators of transcription: STATs-mediated mitochondrial neuroprotection.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanisms and therapeutic prospect of the JAK-STAT signaling pathway in liver cancer.Molecular and cellular biochemistry · 2025Review
- Enhanced thioredoxin, glutathione and Nrf2 antioxidant systems by safflower extract and aceglutamide attenuate cerebral ischaemia/reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Ellagic Acid Ameliorates Renal Ischemic-Reperfusion Injury Through NOX4/JAK/STAT Signaling Pathway.Inflammation · 2020Article
- Functions of the sirtuin deacylase SIRT5 in normal physiology and pathobiology.Critical reviews in biochemistry and molecular biology · 2018Review
- Remote Ischemic Conditioning in Cerebral Diseases and Neurointerventional Procedures: Recent Research Progress.Frontiers in neurology · 2018Review
- Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia.Brain pathology (Zurich, Switzerland) · 2017Article
- microRNA-200a silencing protects neural stem cells against cerebral ischemia/reperfusion injury.PloS one · 2017Article
- Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke.Experimental neurology · 2015Review
- Non-pharmaceutical therapies for stroke: mechanisms and clinical implications.Progress in neurobiology · 2014Review
- Fatty acid methyl esters and Solutol HS 15 confer neuroprotection after focal and global cerebral ischemia.Translational stroke research · 2014Article
- Ischemic preconditioning alters the epigenetic profile of the brain from ischemic intolerance to ischemic tolerance.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Neuroprotection against hypoxia/ischemia: δ-opioid receptor-mediated cellular/molecular events.Cellular and molecular life sciences : CMLS · 2013Review
- Ischemic preconditioning and clinical scenarios.Current opinion in neurology · 2013Review
- Transgenic overexpression of peroxiredoxin-2 attenuates ischemic neuronal injury via suppression of a redox-sensitive pro-death signaling pathway.Antioxidants & redox signaling · 2012Article
- Novel mitochondrial targets for neuroprotection.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Review
- Molecular and cellular pathways as a target of therapeutic hypothermia: pharmacological aspect.Current neuropharmacology · 2012Article
- Effects of Herba epimedii and Fructus ligustri lucidi on the transcription factors in hypothalamus of aged rats.Chinese journal of integrative medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cerebral ischemia is defined as little or no blood flow in cerebral circulation, characterized by low tissue oxygen and glucose levels, which promotes neuronal mitochondria dysfunction leading to cell death. A strategy to counteract cerebral ischemia-induced neuronal cell death is ischemic preconditioning (IPC). IPC results in neuroprotection, which is conferred by a mild ischemic challenge prior to a normally lethal ischemic insult. Although many IPC-induced mechanisms have been described, many cellular and subcellular mechanisms remain undefined. Some reports have suggested key signal transduction pathways of IPC, such as activation of protein kinase C epsilon, mitogen-activated protein kinase, and hypoxia-inducible factors, that are likely involved in IPC-induced mitochondria mediated-neuroprotection. Moreover, recent findings suggest that signal transducers and activators of transcription (STATs), a family of transcription factors involved in many cellular activities, may be intimately involved in IPC-induced ischemic tolerance. In this review, we explore current signal transduction pathways involved in IPC-induced mitochondria mediated-neuroprotection, STAT activation in the mitochondria as it relates to IPC, and functional significance of STATs in cerebral ischemia.
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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.