ReviewProgress in neurobiology2017
Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery.
Review in Progress in neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed.
- Decreased angiogenesis as a possible pathomechanism in cervical degenerative myelopathy.Scientific reports · 2021Trial
- Neuron-derived SPP1 instructs microglia to limit degeneration.Science advances · 2026Article
- Electroacupuncture Promotes Synaptic Recovery After Cerebral Ischemia-Reperfusion by Activating SIRT1 to Inhibit the NF-κB Pathway and Regulate Astrocyte Phenotypic Transformation.Neurochemical research · 2026Article
- Cerebral in situ ischemic postconditioning: From bench to bedside and beyond.Neuroprotection (Chichester, England) · 2026Review
- Article
- Mitigating Early Phosphatidylserine Exposure in a Tmem30a-Dependent Way Ameliorates Neuronal Damages After Ischemic Stroke.MedComm · 2025Article
- Metal nanoparticles in neuroinflammation: impact on microglial dynamics and CNS function.RSC advances · 2025Review
- Chronic Inflammation Offers Hints About Viable Therapeutic Targets for Preeclampsia and Potentially Related Offspring Sequelae.International journal of molecular sciences · 2024Review
- Phosphatidylserine: A Novel Target for Ischemic Stroke Treatment.Biomolecules · 2024Review
- Sustained release of vascular endothelial growth factor A and basic fibroblast growth factor from nanofiber membranes reduces oxygen/glucose deprivation-induced injury to neurovascular units.Neural regeneration research · 2024Article
- Neuroglobin-enriched secretome provides neuroprotection against hydrogen peroxide and mitochondrial toxin-induced cellular stress.Cell stress · 2024Article
- Leveraging single-cell RNA sequencing to unravel the impact of aging on stroke recovery mechanisms in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- An Updated Review of Mitochondrial Transplantation as a Potential Therapeutic Strategy Against Cerebral Ischemia and Cerebral Ischemia/Reperfusion Injury.Molecular neurobiology · 2023Review
- Exploring the therapeutic potential of the mitochondrial transfer-associated enzymatic machinery in brain degeneration.Frontiers in physiology · 2023Review
- Endothelial cells regulate astrocyte to neural progenitor cell trans-differentiation in a mouse model of stroke.Nature communications · 2022Article
- Commentary: Can astrocytic mitochondria therapy be used as antioxidant conditioning to protect neurons?Conditioning medicine · 2022Article
- Lipocalin-2-Mediated Insufficient Oligodendrocyte Progenitor Cell Remyelination for White Matter Injury After Subarachnoid Hemorrhage via SCL22A17 Receptor/Early Growth Response Protein 1 Signaling.Neuroscience bulletin · 2022Article
- Neuron derived fractalkine promotes microglia to absorb hematoma via CD163/HO-1 after intracerebral hemorrhage.Cellular and molecular life sciences : CMLS · 2022Article
- Mitochondrial quality control in acute ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes.Translational stroke research · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Self-preservation is required for life. At the cellular level, this fundamental principle is expressed in the form of molecular mechanisms for preconditioning and tolerance. When the cell is threatened, internal cascades of survival signaling become triggered to protect against cell death and defend against future insults. Recently, however, emerging findings suggest that this principle of self-preservation may involve not only intracellular signals; the release of extracellular signals may provide a way to recruit adjacent cells into an amplified protective program. In the central nervous system where multiple cell types co-exist, this mechanism would allow threatened neurons to "ask for help" from glial and vascular compartments. In this review, we describe this new concept of help-me signaling, wherein damaged or diseased neurons release signals that may shift glial and vascular cells into potentially beneficial phenotypes, and help remodel the neurovascular unit. Understanding and dissecting these non-cell autonomous mechanisms of self-preservation in the CNS may lead to novel opportunities for neuroprotection and neurorecovery.
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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.