ArticleEBioMedicine2015
Hypothermic Preconditioning of Human Cortical Neurons Requires Proteostatic Priming.
Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
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- Adaptive inter-tissue proteostasis networks in aging and neurodegeneration.Bioscience reports · 2026Review
- Circadian Control of Protein Synthesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Therapeutic modulation of protein RBM3 for ischemic stroke treatment.Frontiers in pharmacology · 2025Review
- Circadian regulation of macromolecular complex turnover and proteome renewal.The EMBO journal · 2024Article
- Redox regulation of UPR signalling and mitochondrial ER contact sites.Cellular and molecular life sciences : CMLS · 2024Review
- Protective Effects and Mechanisms of Inhibiting Endoplasmic Reticulum Stress on Cold Seawater Immersion Combined with Hemorrhagic Shock.Journal of inflammation research · 2024Article
- Article
- HNRNPH1 regulates the neuroprotective cold-shock protein RBM3 expression through poison exon exclusion.The EMBO journal · 2023Article
- RNA-Binding Proteins in Bladder Cancer.Cancers · 2023Review
- Understanding the Function and Mechanism of Zebrafish Tmem39b in Regulating Cold Resistance.International journal of molecular sciences · 2022Article
- Hypothermia Alleviates Reductive Stress, a Root Cause of Ischemia Reperfusion Injury.International journal of molecular sciences · 2022Article
- Change in Oxidative Stress and Mitochondrial Dynamics in Response to Elevated Cold-Inducible RNA-Binding Protein in Cardiac Surgery-Associated Acute Kidney Injury.Oxidative medicine and cellular longevity · 2022Article
- Mild cold stress specifically disturbs clustering movement of DFCs and sequential organ left-right patterning in zebrafish.Frontiers in cell and developmental biology · 2022Article
- microRNA-33 maintains adaptive thermogenesis via enhanced sympathetic nerve activity.Nature communications · 2021Article
- Review
- Cold-induced chromatin compaction and nuclear retention of clock mRNAs resets the circadian rhythm.The EMBO journal · 2020Article
- The S100B Protein and Partners in Adipocyte Response to Cold Stress and Adaptive Thermogenesis: Facts, Hypotheses, and Perspectives.Biomolecules · 2020Review
- Limited Oxidative Stress Favors Resistance to Skeletal Muscle Atrophy in Hibernating Brown Bears (Antioxidants (Basel, Switzerland) · 2019Article
- Extracellular CIRP (eCIRP) and inflammation.Journal of leukocyte biology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypothermia is potently neuroprotective but poor mechanistic understanding has restricted its clinical use. Rodent studies indicate that hypothermia can elicit preconditioning, wherein a subtoxic cellular stress confers resistance to an otherwise lethal injury. The molecular basis of this preconditioning remains obscure. Here we explore molecular effects of cooling using functional cortical neurons differentiated from human pluripotent stem cells (hCNs). Mild-to-moderate hypothermia (28-32 °C) induces cold-shock protein expression and mild endoplasmic reticulum (ER) stress in hCNs, with full activation of the unfolded protein response (UPR). Chemical block of a principal UPR pathway mitigates the protective effect of cooling against oxidative stress, whilst pre-cooling neurons abrogates the toxic injury produced by the ER stressor tunicamycin. Cold-stress thus preconditions neurons by upregulating adaptive chaperone-driven pathways of the UPR in a manner that precipitates ER-hormesis. Our findings establish a novel arm of neurocryobiology that could reveal multiple therapeutic targets for acute and chronic neuronal injury.
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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.