ArticleNature communications2025
SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Developmental expression patterns of neuronal growth genes across human brain stages using Bgee transcriptomic data.IBRO neuroscience reports · 2026Article
- A Microenvironment-Adaptive Scaffold Rejuvenates Peripheral Nerve Regeneration During Aging Via Dual Modulation of Ferroptotic Stimuli in Schwann Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026Review
- Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
During peripheral nerve (PN) development, unmyelinated axons (nmAs) tightly fasciculate before being separated and enveloped by non-myelinating Schwann cells (nmSCs), glial cells essential for maintaining nmA integrity. How such a switch from axon-axon to axon-glia interactions is achieved remains poorly understood. Here, we find that inactivating SC-derived SEMA3B or its axonal receptor components in mice leads to incomplete nmA separation and envelopment by nmSCs, eliciting hyperalgesia and allodynia. Conversely, increasing SEMA3B levels in SCs accelerates nmA separation and envelopment. SEMA3B transiently promotes nmA defasciculation accompanied by cell adhesion molecule (CAM) endocytosis, subsequently facilitating nmA-nmSC association. Restoring SEMA3B expression following PN injury promotes nmA-nmSC re-association and alleviates hyperalgesia and allodynia. We propose that SEMA3B-induced CAM turnover facilitates a switch from axon-axon to axon-glia interactions promoting nmA envelopment by nmSCs, which may be exploitable for alleviating PN injury-induced pain by accelerating the restoration of nmA integrity.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.