ReviewNeurochemistry international2019
Impaired capacity to restore proteostasis in the aged brain after ischemia: Implications for translational brain ischemia research.
Review in Neurochemistry international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Dynamic Oxidative States: Interplay of Aging, Metabolic Stress, and Circadian Rhythms in Modulating Stroke Severity.Antioxidants (Basel, Switzerland) · 2025Review
- Activation of ATF6 Signaling Confers Long-Term Beneficial Effects in Young and Aged Mice After Permanent Stroke.Translational stroke research · 2025Article
- Activation of the PERK/MANF/STAT3 Pathway in Astrocytes Promotes Synaptic Remodeling and Neurological Recovery in the Acute Phase After Stroke in Mice.Neural plasticity · 2025Article
- Therapeutic Potential of Targeting the PERK Signaling Pathway in Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting O-GlcNAcylation in ischemic stroke.Neural regeneration research · 2022Article
- Beneficial effects of neuronal ATF6 activation in permanent ischemic stroke.Frontiers in cellular neuroscience · 2022Article
- Remote but not Distant: a Review on Experimental Models and Clinical Trials in Remote Ischemic Conditioning as Potential Therapy in Ischemic Stroke.Molecular neurobiology · 2022Review
- An update on the unfolded protein response in brain ischemia: Experimental evidence and therapeutic opportunities.Neurochemistry international · 2021Review
- Activation of the ATF6 (Activating Transcription Factor 6) Signaling Pathway in Neurons Improves Outcome After Cardiac Arrest in Mice.Journal of the American Heart Association · 2021Article
- Increasing O-GlcNAcylation is neuroprotective in young and aged brains after ischemic stroke.Experimental neurology · 2021Article
- Translation Regulation by eIF2α Phosphorylation and mTORC1 Signaling Pathways in Non-Communicable Diseases (NCDs).International journal of molecular sciences · 2020Review
- Article
- Proteostasis During Cerebral Ischemia.Frontiers in neuroscience · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Brain ischemia induced by cardiac arrest or ischemic stroke is a severe form of metabolic stress that substantially disrupts cellular homeostasis, especially protein homeostasis (proteostasis). As proteostasis is fundamental for cellular and organismal health, cells have developed a complex network to restore proteostasis impaired by stress. Many components of this network - including ubiquitination, small ubiquitin-like modifier (SUMO) conjugation, autophagy, and the unfolded protein response (UPR) - are activated in the post-ischemic brain, and play a crucial role in cell survival and recovery of neurologic function. Importantly, recent studies have shown that ischemia-induced activation of these proteostasis-related pathways in the aged brain is impaired, indicating an aging-related decline in the self-healing capacity of the brain. This impaired capacity is a significant factor for consideration in the field of brain ischemia because the vast majority of cardiac arrest and stroke patients are elderly. In this review, we focus on the effects of aging on these critical proteostasis-related pathways in the brain, and discuss their implications in translational brain ischemia research.
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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.