ReviewFrontiers in neuroscience2019
Proteostasis During Cerebral Ischemia.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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
26 citing papers in PubMed, 49 citations in OpenAlex.
- Alpha-Synuclein Dynamics in Cerebral Ischemia.ASN neuro · 2026Review
- Dynamic Oxidative States: Interplay of Aging, Metabolic Stress, and Circadian Rhythms in Modulating Stroke Severity.Antioxidants (Basel, Switzerland) · 2025Review
- Autophagy hub-protein p62 orchestrates oxidative, endoplasmic reticulum stress, and inflammatory responses post-ischemia, exacerbating stroke outcome.Redox biology · 2025Article
- Impact of ATF6 deletion on the embryonic brain development.iScience · 2025Article
- RiboTag RNA Sequencing Identifies Local Translation of HSP70 in Astrocyte Endfeet After Cerebral Ischemia.International journal of molecular sciences · 2025Article
- Neuroprotective Effects of Chaperonin Containing TCP1 Subunit 2 (CCT2) on Motor Neurons Following Oxidative or Ischemic Stress.Neurochemical research · 2024Article
- Obesity and Environmental Risk Factors Significantly Modify the Association between Ischemic Stroke and the Hero ChaperoneLife (Basel, Switzerland) · 2024Article
- The Role of Induced Pluripotent Stem Cells in the Treatment of Stroke.Current neuropharmacology · 2024Review
- Plasma neurofilament light chain associated with impaired regional cerebral blood flow in healthy individuals.Current journal of neurology · 2023Article
- Reinventing the Penumbra - the Emerging Clockwork of a Multi-modal Mechanistic Paradigm.Translational stroke research · 2023Review
- ATF6β Deficiency Elicits Anxiety-like Behavior and Hyperactivity Under Stress Conditions.Neurochemical research · 2023Article
- Polymorphism ofIBRO neuroscience reports · 2023Article
- Cochlear implantation impairs intracochlear microcirculation and counteracts iNOS induction in guinea pigs.Frontiers in cellular neuroscience · 2023Article
- Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism.Frontiers in pharmacology · 2023Review
- Markers and mechanisms of death inFrontiers in aging · 2023Article
- Exacerbated VEGF up-regulation accompanies diabetes-aggravated hemorrhage in mice after experimental cerebral ischemia and delayed reperfusion.Neural regeneration research · 2022Article
- Thrombolysis by PLAT/tPA increases serum free IGF1 leading to a decrease of deleterious autophagy following brain ischemia.Autophagy · 2022Article
- Unveiling OASIS family as a key player in hypoxia-ischemia cases induced by cocaine using generative adversarial networks.Scientific reports · 2022Article
- Dysregulation of mTOR Signaling after Brain Ischemia.International journal of molecular sciences · 2022Review
- A novel link between silent information regulator 1 and autophagy in cerebral ischemia-reperfusion.Frontiers in neuroscience · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in the regulation of proteostasis: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however, their over-activation in duration or intensity can lead to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. A better understanding of autophagy and ER stress will allow the development of therapeutic strategies for stroke, both at the acute phase and during recovery. This review summarizes the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. We argue that the processes governing proteostasis should be considered together in stroke, rather than focusing either on ER stress or autophagy in isolation.
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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.