ArticleFrontiers in molecular neuroscience2026
Dynamic transcriptomic profiling of dorsal root ganglia reveals stage-specific mechanisms in diabetic neuropathic pain.
Article in Frontiers in molecular neuroscience, 2026. 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic peripheral neuropathy (DPN) is the main clinical challenge faced by patients in the middle and advanced stages of diabetes. Due to the unclear cellular and molecular mechanisms, despite decades of in-depth research, its treatment methods are still limited. This study delineates the dynamic transcriptomic landscape of dorsal root ganglia (DRG) in streptozotocin (STZ)-induced diabetic male rats, integrating behavioral phenotyping and cross-model comparisons. We observed phenotypic heterogeneity, with only 60% of STZ-treated rats developing diabetic neuropathic pain (DNP group). In comparison, 37% remained pain-free (non-DNP group) despite comparable hyperglycemia and weight loss. RNA sequencing revealed stage-specific molecular signatures: early DNP (4 weeks post-STZ) involved PI3K-Akt/Ras signaling pathways, whereas late DNP (8 weeks) implicated several virus infection and neuroactive ligand-receptor pathways. Strikingly, 72% of differentially expressed genes (DEGs) at 8 weeks were unique to chronic DNP maintenance. Cross-model analysis demonstrated little overlap between DNP, bone cancer pain, and nerve injury models (<1% shared DEGs), with only Serpina3n universally upregulated. Functional annotations highlighted dysregulated extracellular matrix remodeling, immune receptor activity, and virus-related pathways unique to DNP progression. These findings reveal (1) intrinsic phenotypic variability in diabetic neuropathy progression, (2) temporally distinct pathogenic mechanisms governing DNP initiation versus persistence, and (3) a unique transcriptional fingerprint distinguishing DNP from other neuropathic pain etiologies. This work provides a roadmap for stage-specific therapeutic targeting and underscores the necessity of precision approaches in diabetic neuropathy management.
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.