ArticleFrontiers in cellular neuroscience2018
Mitochondrial Damage-Associated Molecular Patterns of Injured Axons Induce Outgrowth of Schwann Cell Processes.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 16 citations in OpenAlex.
- Endogenous Trigeminal Neurons Induce Schwann Differentiation of Donor Stem Cells in Dental Pulp Regeneration via Reciprocal Extracellular Vesicles Interplay.Exploration (Beijing, China) · 2026Article
- Wallerian Degeneration and Nerve Regeneration-A Review of Cellular and Molecular Events.International journal of molecular sciences · 2026Review
- The Role of Vitamin D in Neuropathic Pain: Biological Mechanisms and Clinical Relevance.International journal of molecular sciences · 2026Review
- Bioactive Compounds as Modulators of N-Formyl Peptide Signaling in Chronic Diseases.Molecules (Basel, Switzerland) · 2025Review
- Annexin A1 in the nervous and ocular systems.Neural regeneration research · 2024Review
- TFAM deficiency in dendritic cells leads to mitochondrial dysfunction and enhanced antitumor immunity through cGAS-STING pathway.Journal for immunotherapy of cancer · 2023Article
- Neuroscience of Peripheral Nerve Regeneration.Journal of pharmacy & bioallied sciences · 2021Review
- Toll-Like Receptor 9-Mediated Neuronal Innate Immune Reaction Is Associated with Initiating a Pro-Regenerative State in Neurons of the Dorsal Root Ganglia Non-Associated with Sciatic Nerve Lesion.International journal of molecular sciences · 2021Article
- The Role of Formyl Peptide Receptors in Neurological Diseases via Regulating Inflammation.Frontiers in cellular neuroscience · 2021Review
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
- Article
- TheNeural regeneration research · 2020Review
- Curse of the devil: molecular insights into the emergence of transmissible cancers in the Tasmanian devil (Sarcophilus harrisii).Cellular and molecular life sciences : CMLS · 2020Review
- Role of formyl peptide receptor 2 (FPR2) in the normal brain and in neurological conditions.Neural regeneration research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activated Schwann cells put out cytoplasmic processes that play a significant role in cell migration and axon regeneration. Following nerve injury, axonal mitochondria release mitochondrial damage-associated molecular patterns (mtDAMPs), including formylated peptides and mitochondrial DNA (mtDNA). We hypothesize that mtDAMPs released from disintegrated axonal mitochondria may stimulate Schwann cells to put out cytoplasmic processes. We investigated RT4-D6P2T schwannoma cells (RT4)
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.