Integrative analysis identifies Hspa5 as a key regulator of the ERS/UPR-immune axis in spinal cord injury.
Overview
- School of Clinical Medicine, Ningxia Medical University, Yinchuan, China
- Ningxia Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, China
- The First Clinical College, The First Affiliated Hospital, Hainan Medical University, Haikou, China
- Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, China
Abstract
Background: Endoplasmic reticulum stress (ERS) and the unfolded protein response (UPR) are critical in secondary spinal cord injury (SCI), but their systematic characterization and link to immune infiltration remain unclear. This study aimed to identify key ERS/
Methods: We analyzed bulk RNA-seq data (GSE151371) to identify differentially expressed genes (DEGs), followed by pathway enrichment analyses. Machine learning (SVM-RFE) and protein-protein interaction networks were used to screen for hub genes. The identified hub genes were validated using an independent cohort (GSE5296), single-cell sequencing data (GSE213240), and qRT-PCR in a murine SCI model.
Results: We identified 17 ERS-related and 27 UPR-related DEGs, primarily enriched in neuron death pathways. SCI samples showed elevated ERS/
Conclusion: ERS/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Data links
- ncbi.nlm.nih.gov/
geo , NCBI; found in “Data availability statement”
Data availability statement
Publicly available datasets were analyzed in this study. This data can be found here: The datasets (GSE151371, GSE5296, and GSE213240) used in this study are available in the GEO database (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, pages, dates, 3 authors, 5 keywords, 55 references.
Cite
This paper
He, G., Yang, A., & Xia, H. (2026). Integrative analysis identifies Hspa5 as a key regulator of the ERS/
BibTeX
@article{he2026integrati
author = {He, Guoyuan and Yang, Aichun and Xia, Hechun},
title = {{Integrative analysis identifies Hspa5 as a key regulator of the ERS/
journal = {Frontiers in genetics},
year = {2026},
month = jun,
volume = {17},
pages = {1833119},
publisher = {Frontiers Media SA},
issn = {1664-8021},
doi = {10.3389/
url = {https://
pmid = {42394947},
pmcid = {PMC13327658}
}
RIS
TY - JOUR
AU - He, Guoyuan
AU - Yang, Aichun
AU - Xia, Hechun
TI - Integrative analysis identifies Hspa5 as a key regulator of the ERS/
T2 - Frontiers in genetics
J2 - Front Genet
PY - 2026
DA - 2026/
VL - 17
SP - 1833119
SN - 1664-8021
PB - Frontiers Media SA
DO - 10.3389/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.3389/
"type": "article-journal",
"title": "Integrative analysis identifies Hspa5 as a key regulator of the ERS/
"container-title": "Frontiers in genetics",
"author": [
{
"family": "He",
"given": "Guoyuan"
},
{
"family": "Yang",
"given": "Aichun"
},
{
"family": "Xia",
"given": "Hechun"
}
],
"container-title-short":
"volume": "17",
"page": "1833119",
"DOI": "10.3389/
"PMID": "42394947",
"PMCID": "PMC13327658",
"ISSN": "1664-8021",
"publisher": "Frontiers Media SA",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
19
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1096/fj.202504890rr
- Purinergic Receptor P2Y2 Regulates Neurogenesis and Functional Recovery Following Spinal Cord Injury in Zebrafish.Journal: FASEB journal : official publication of the Federation of American Societies for Experimental BiologyIn common: other condition, 2 references
- [2] doi:10.3390/ijms27156671
- Inflamed Yet Immune-Evasive? A Transcriptomic Meta-Analysis Identifies Conserved Inflammatory, Developmental, and Neuronal Signatures Associated with Polyploid Giant Cancer Cells.Journal: International journal of molecular sciencesIn common: genetics / omics, other condition, cellular / molecular, 1 reference
- [3] doi:10.1371/journal.pcbi.1014573 [code]
- Cell-type-specific m1A dynamics are associated with microglial phenotypic transition and neuronal metabolic adaptation during spinal cord injury.Journal: PLoS computational biologyIn common: genetics / omics, other condition, cellular / molecular, 1 reference
- [4] doi:10.3390/ijms27135711
- Role of Supraspinal Neuroinflammation in Chronic Pain After Experimental Spinal Cord Injury-A Systematic Review.Journal: International journal of molecular sciencesIn common: other condition, cellular / molecular, 1 reference
- [5] doi:10.1002/cns.70834
- Wnt5a-Induced Exosomes From Bone Marrow Mesenchymal Stem Cells Promote Spinal Cord Injury Repair by Modulating Immune Cell Phenotypes and Alleviating Neuroinflammation via the NF-κB Pathway.Journal: CNS neuroscience & therapeuticsIn common: other condition, cellular / molecular, 1 reference
- [6] doi:10.1038/s42003-026-10226-8 [code]
- Discovery of a pyrazolopyridine alkaloid that mitigates neuronal ER stress and age-related decline.Journal: Communications biologyIn common: other condition, 1 reference
- [7] doi:10.1007/s12035-026-05792-1
- Identification and Experimental Validation of Biomarkers Associated with PI3K/
AKT Signaling Pathway in Spinal Cord Injury. Journal: Molecular neurobiologyIn common: other condition, 1 reference - [8] doi:10.3389/fnmol.2026.1817096 [code]
- EIF2S1-PELO co-expression architecture in human brain: pairing-family decomposition reveals constitutive transcriptional coupling and functional layer separation.Journal: Frontiers in molecular neuroscienceIn common: genetics / omics, 1 reference
- [9] doi:10.1016/j.jbc.2026.113363
- The Src family kinase YES regulates DNAJB6b chaperone activity to modulate tau aggregation in Alzheimer's disease.Journal: The Journal of biological chemistryIn common: cellular / molecular, 1 reference
- [10] doi:10.1242/dev.205386
- Loss of the endoplasmic reticulum protein canopy 1 disrupts the function and circuit organization of V2R-expressing vomeronasal sensory neurons.Journal: Development (Cambridge, England)In common: cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
