ReviewMolecular pain
Precursor signaling redefined: Proneurotrophin-3, not neurotrophin-3, in primary sensory neurons as an instigator in neuropathic pain.
Review in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Neurotrophin-3 (NT3), one member of the nerve growth factor family of neurotrophins, is initially synthesized as a large precursor, termed proneurotrophin-3 (proNT3), which undergoes proteolytic cleavage to generate mature NT3. A growing body of evidence suggests that proNT3 and its mature form, NT3, have opposing roles in the nervous system. A systematic literature search of PubMed was conducted using predefined search terms related to NT3, proNT3, expression, dorsal root ganglion (DRG), and pain. The role of NT3 in neuropathic pain has been debated in earlier studies. Importantly, more recent studies have shown that proNT3, rather than NT3, is expressed in the DRG. In this review, we delineate the expression and distribution pattern of proNT3 in primary sensory neurons of the DRG under normal conditions, as well as its upregulation in injured DRG following peripheral nerve injury. We highlight that DRG proNT3 upregulation is required for the development and maintenance of neuropathic pain and discuss the role of C-C chemokine ligand 2 in mediating the contribution of proNT3-triggered TrkC activation to neuropathic pain in the DRG.
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.