ReviewFrontiers in neurology2015
Novel Cellular Mechanisms for Neuroprotection in Ischemic Preconditioning: A View from Inside Organelles.
Review in Frontiers in neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Brain Ischemic Tolerance Triggered by Preconditioning Involves Modulation of Tumor Necrosis Factor-α-Stimulated Gene 6 (TSG-6) in Mice Subjected to Transient Middle Cerebral Artery Occlusion.Current issues in molecular biology · 2024Article
- Oxidative Metabolism in Brain Ischemia and Preconditioning: Two Sides of the Same Coin.Antioxidants (Basel, Switzerland) · 2024Review
- Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia.International journal of molecular sciences · 2024Review
- Evaluation of prophylactic efficacy of sodium thiosulfate in combating I/R injury in rat brain: exploring its efficiency further in vascular calcified brain slice model.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Cerebral Ischemic Preconditioning Aggravates Death of Oligodendrocytes.Biomolecules · 2022Article
- Ischemic Preconditioning Modulates the Peripheral Innate Immune System to Promote Anti-Inflammatory and Protective Responses in Mice Subjected to Focal Cerebral Ischemia.Frontiers in immunology · 2022Article
- Preconditioning-Activated AKT Controls Neuronal Tolerance to Ischemia through the MDM2-p53 Pathway.International journal of molecular sciences · 2021Article
- Refocusing the Brain: New Approaches in Neuroprotection Against Ischemic Injury.Neurochemical research · 2021Review
- Positive and negative conditioning in the neonatal brain.Conditioning medicine · 2018Article
- UBIAD1 protects against oxygen-glucose deprivation/reperfusion-induced multiple subcellular organelles injury through PI3K/AKT pathway in N2A cells.Journal of cellular physiology · 2018Article
- Non-coding RNAs and neuroprotection after acute CNS injuries.Neurochemistry international · 2017Review
- Global ablation of the mitochondrial calcium uniporter increases glycolysis in cortical neurons subjected to energetic stressors.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Structure-based dynamic arrays in regulatory domains of sodium-calcium exchanger (NCX) isoforms.Scientific reports · 2017Article
- Metabolic features of chronic fatigue syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Ischemic preconditioning inhibits over-expression of arginyl-tRNA synthetase gene Rars in ischemia-injured neurons.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Endothelin Receptors, Mitochondria and Neurogenesis in Cerebral Ischemia.Current neuropharmacology · 2016Review
- Reconciling the IPC and Two-Hit Models: Dissecting the Underlying Cellular and Molecular Mechanisms of Two Seemingly Opposing Frameworks.Journal of immunology research · 2015Review
- Safety and efficacy of remote ischemic conditioning in pediatric moyamoya disease patients treated with revascularization therapy.Brain circulationArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic preconditioning represents an important adaptation mechanism of CNS, which results in its increased tolerance to the lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and not yet completely clarified. In the last 10 years, great attention has been devoted to unravel the intracellular pathways activated by preconditioning and responsible for the establishing of the tolerant phenotype. Indeed, recent papers have been published supporting the hypothesis that mitochondria might act as master regulators of preconditioning-triggered endogenous neuroprotection due to their ability to control cytosolic calcium homeostasis. More interestingly, the demonstration that functional alterations in the ability of mitochondria and endoplasmic reticulum (ER) managing calcium homeostasis during ischemia, opened a new line of research focused to the role played by mitochondria and ER cross-talk in the pathogenesis of cerebral ischemia in order to identify new molecular mechanisms involved in the ischemic tolerance. In line with these findings and considering that the expression of the three isoforms of the sodium calcium exchanger (NCX), NCX1, NCX2, and NCX3, mainly responsible for the regulation of Ca(2+) homeostasis, was reduced during cerebral ischemia, it was investigated whether these proteins might play a role in neuroprotection induced by ischemic tolerance. In this review, evidence supporting the involvement of ER and mitochondria interaction within the preconditioning paradigm will be provided. In particular, the key role played by NCXs in the regulation of Ca(2+)-homeostasis at the different subcellular compartments will be discussed as new molecular mechanism proposed for the establishing of ischemic tolerant phenotype.
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