ArticleJournal of translational medicine2026
PPM1A dysfunction aggravates DPN pathology through NF-κB/NLRP3/p-tau axis involving Schwann cell/DRG neuron crosstalk.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Otilonium bromide ameliorates paclitaxel-induced peripheral neuropathy by targeting phosphatase PPM1A.Journal of neuroinflammation · 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
8 authors.
Funding
Abstract
backgroundDiabetic peripheral neuropathy (DPN) is a severe diabetic complication with complex pathogenesis. Hyperphosphorylation of tau (p-tau) and neuroinflammation are tightly associated with DPN pathology, although the underlying mechanisms remain obscure.
methodsPhosphoproteomics assay with biological verification was performed against the sciatic nerve (SN) tissues from DPN patients and normal individuals to explore the key phosphoprotein(s) involved in DPN pathology. Based on these findings, biological assays including in vivo phosphoprotein-knockdown were then carried out to verify the determined phosphoprotein-mediated mechanisms in DPN pathology against the SN tissues/dorsal root ganglion (DRG) of the model mice.
resultsProtein phosphatase Mg²⁺/Mn²⁺ dependent 1 A (PPM1A) enzyme activity was abnormally reduced in both DPN patients and model mice. Treatment with Miltefosine (MF), a PPM1A activator, effectively improved the DPN-like pathology in mice. PPM1A dysfunction aggravates DPN pathology through NF-κB/NLRP3/p-tau axis involving Schwann cell/DRG neuron crosstalk.
conclusionOur results highlight the close linkage of PPM1A dysfunction to DPN pathology and suggest that pharmacological activation of PPM1A is a potential therapeutic tactic for DPN, while MF shows promise as a valuable drug lead compound against DPN.
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.