Evidence map›Paper›PMID 41437123›Full record

ArticleActa neuropathologica communications2025

Removal or inhibition of transglutaminase 2 decreases cellular stress, supporting tissue preservation, and recovery after SCI.

Mousumi Ghosh, Omar Elwardany, Xiaoqi Pan, Shannon Jacqueline Saigh, Damien D Pearse

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Mousumi GhoshThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, 33136, USA. mghosh@med.miami.edu.
Omar ElwardanyThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Xiaoqi PanThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Shannon Jacqueline SaighDepartment of Surgery-Oncology, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Damien D PearseThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.

Funding

Tumor Biology Research ProgramP30CA240139 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Stephen D. Nimer · 2019 to 2026
$24.1M
NCI NIH HHS P30 CA240139State of Florida Department of Health Bankhead-Coley Cancer Research Program FL DOH 8BC09The Buoniconti Fund and The Miami Project to Cure Paralysis Not ApplicableThe Buoniconti Fund and The Miami Project to Cure Paralysis and The John M. and Jocelyn H.K. Watkins Distinguished Chair in Cell Therapies Not ApplicableThe Flow Cytometry Shared Resource (FCSR) of the Sylvester Comprehensive Cancer Center at the University of Miami Not ApplicableThe Miami Project to Cure Paralysis Not ApplicableThe National Cancer Institute (NCI) of the National Institutes of Health (NIH) P30CA240139
6 · The paper itself

Abstract

Transglutaminase 2 (TG2) is a multifunctional enzyme widely implicated in neuroinflammation and extracellular matrix (ECM) remodeling after central nervous system (CNS) injury and diseases. In spinal cord injury (SCI), TG2 contributes significantly to pathology through ECM remodeling and glial scar formation. Here, we explored the intracellular roles of TG2 following severe spinal cord compression injury, utilizing TG2 knockout (KO) mice and pharmacological inhibition via cystamine. Genetic deletion or inhibition of TG2 significantly improved locomotor function and promoted enhanced preservation of white and gray matter post-injury. Mechanistically, TG2 KO reduced fibronectin deposition, chondroitin sulfate proteoglycan accumulation, and reactive gliosis. Importantly, imaging mass cytometry revealed that TG2 deletion attenuated cellular stress responses, including reductions in ER stress markers (GRP78), oxidative stress mediators (pNrf2), mitochondrial dysfunction indicators (BNIP3 and cytochrome c), and increased neuronal expression of survival-associated (pREL-NFκB). These results highlight a novel intracellular function for TG2 in exacerbating neurodegeneration through modulation of cellular stress pathways, offering promising therapeutic implications for SCI recovery.

Indexed as

GTP-Binding ProteinsRecovery of FunctionSpinal Cord InjuriesTransglutaminasesAnimalsCystamineEndoplasmic Reticulum Chaperone BiPFemaleFibronectinsGliosisMiceMice, Inbred C57BLMice, KnockoutProtein Glutamine gamma Glutamyltransferase 2CystamineEndoplasmic Reticulum Chaperone BiPFibronectinsGTP-Binding ProteinsHspa5 protein, mouseProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesAxonal regenerationCellular stressClip compression injuryGlial scar formationImaging mass cytometryLocomotor recoveryNeuroprotectionSpinal cord injuryTransglutaminase 2

Identifiers

PMID41437123
PMCPMC12836936

What OpenQuestion holds

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Registered trials

None linked

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.