ArticleThe Kaohsiung journal of medical sciences2026
Role of COL1A1 and CD44 in Modulating JAK1/STAT3-Mediated Autophagy for Spinal Cord Injury Recovery.
Article in The Kaohsiung journal of medical sciences, 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.
- Role of COL1A1 and CD44 in Modulating JAK1/STAT3-Mediated Autophagy for Spinal Cord Injury Recovery.The Kaohsiung journal of medical sciences · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a severe trauma to the central nervous system that often leads to motor and sensory dysfunction in patients, severely affecting their quality of life. Autophagy plays a role in the pathological process of SCI, but the specific mechanism of autophagy in this case is unknown. COL1A1 and CD44, as potentially important genes in the autophagic process, may regulate the signaling pathway and thus affect the autophagic process through protein interactions. The aim of this study was to investigate the interaction between COL1A1 and CD44 and its mechanism of regulating autophagy through the JAK1/STAT3 pathway, providing new targets for SCI treatment. An SCI rat model was established, along with a PC12 cell model induced by oxygen-glucose deprivation (OGD). COL1A1 and CD44 in rat spinal cord tissues and cells were assessed using RT-qPCR and Western blot. Motor function in rats was assessed by BBB score, and the pathological conditions of the rat spinal cord tissues and neuronal numbers were observed by HE staining and Nissl staining. COL1A1 and CD44 localization in PC12 cells was confirmed via immunofluorescence analysis, and their targeting binding was verified by Co-IP. In the cell model, apoptosis, proliferation, and autophagy were evaluated through flow cytometry, CCK-8, and mRFP-GFP-LC3 transfection, respectively. The activation of the JAK1/STAT3 cascade in spinal cord tissues and PC12 cells was assessed, along with its function in the cell model. COL1A1 and CD44 were significantly overexpressed in spinal cord tissues of SCI rats and OGD-treated PC12 cells. COL1A1 silencing promoted functional recovery and autophagy after SCI in rats, ameliorated OGD-induced PC12 cell injury, upregulated autophagy proteins, and increased the number of autophagosomes and autolysosomes. COL1A1 was able to bind to CD44 in a targeting fashion and regulated the JAK1/STAT3 cascade. CD44 overexpression counteracted the positive effects of COL1A1 silencing on both the functional recovery of SCI rats and OGD-induced PC12 cell injury. COL1A1 targets and binds to CD44 to activate autophagy mediated by the JAK1/STAT3 signaling pathway, inhibiting functional recovery after 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.