ArticleFrontiers in genetics2026
Multi-omics identifies a VIM-associated microglial program linked to lactylation, ferroptosis, and neuroinflammation after spinal cord injury.
Article in Frontiers in genetics, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The secondary injury cascade following spinal cord injury (SCI) involves substantial metabolic reprogramming and immune responses. However, whether transcriptional signatures related to lactylation, ferroptosis, and neuroinflammation show coordinated changes after SCI, and which cellular states are associated with these signatures, remain unclear. Methods: Public bulk transcriptomic datasets (GSE47681 and GSE5296) and a single-cell RNA-seq dataset (GSE162610) were integrated. Bioinformatic analyses included single-sample gene set enrichment analysis (ssGSEA), weighted gene co-expression network analysis (WGCNA), protein-protein interaction analysis, pseudotime trajectory inference, and Results: Bulk transcriptomic analysis revealed coordinated elevation of lactylation-related, ferroptosis-related, and inflammation-related signature scores after SCI, with the highest scores observed at 3 days post-injury. Single-cell RNA-seq localized these signatures predominantly to expanded disease-associated microglia (DAM)-like states. Network screening prioritized vimentin (Vim) as a candidate hub gene associated with the three signatures, and Vim-high pathological microglia exhibited an activated inflammatory-metabolic transcriptional state. In the SCI mouse model, VIM, pan-lysine lactylation (pan-Kla), acyl-CoA synthetase long-chain family member 4 (ACSL4), and interleukin-1β (IL-1β) were upregulated in whole-lesion spinal cord tissue. Immunofluorescence further showed increased VIM, pan-Kla, and ACSL4 signals with spatial overlap within IBA1-positive cells after SCI. Conclusion: Pathological DAM-like microglia represent major microglial states exhibiting concurrent lactylation-related, ferroptosis-related, and inflammatory signatures after SCI. VIM was prioritized as a candidate hub associated with this pathological microglial program. These findings provide a cellular and molecular framework for future mechanistic studies of secondary SCI.
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.