Evidence map›Paper›PMID 39909217›Full record

ArticleExperimental neurology2025

Combined treatment targeting Ca2+ store mediated Ca2+ release and store-operated calcium entry reduces secondary axonal degeneration and improves functional outcome after SCI.

Emma Jones, Spencer O Ames, Jesse Brooks, Johnny Morehouse, Norah Hill, Katsuhiko Mikoshiba, Akinobu Suzuki, David P Stirling

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Emma JonesKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Spencer O AmesKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Jesse BrooksKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Johnny MorehouseKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Norah HillKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Katsuhiko MikoshibaShanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai 201210, China; Faculty of Science, Toho University, Funabashi-shi, Chiba-ken 274-8510, Japan; RIKEN Center for Brain Science, Wako-shi, Saitama 351-0198, Japan.
Akinobu SuzukiFaculty of Science, Toho University, Funabashi-shi, Chiba-ken 274-8510, Japan.
David P StirlingKentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA; Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, KY 40202, USA; Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: david.stirling@louisville.edu.

Funding

The role of SOCE in microglia and secondary degeneration after SCIR01NS129987 · NINDS · UNIVERSITY OF LOUISVILLE · PI David Paul Stirling · 2023 to 2026
$1.8M
NINDS NIH HHS R01 NS129987
6 · The paper itself

Abstract

Store-operated calcium entry (SOCE) is crucial for cellular processes, including cellular calcium homeostasis and signaling. However, uncontrolled activation of SOCE is implicated in neurological disorders and CNS trauma, but underlying mechanisms remain unclear. We hypothesized that inhibiting SOCE enhances neurological recovery following contusive spinal cord injury (SCI). To investigate key SOCE effectors, stromal interaction molecules (STIM) and Orai channels on neurological recovery following spinal cord injury (SCI), we utilized male and female conditional neuronal Stim1KO mice to investigate the role of neuronal STIM1 in SCI outcome following a mild (30 kdyn) contusion at T13. To investigate Ca2+ store mediated Ca2+ store depletion, and SOCE-mediated refilling in SCI outcome, we inhibited the IP

Indexed as

AxonsCalciumCalcium SignalingNerve DegenerationRecovery of FunctionSpinal Cord InjuriesAnimalsBoron CompoundsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutStromal Interaction Molecule 1Treatment OutcomeBoron CompoundsCalciumStim1 protein, mouseStromal Interaction Molecule 1Axonal degenerationAxoplasmic reticulumIP(3)ROraiSpinal cord injuryStore-operated calcium entry (SOCE)Stromal interaction molecule proteins (STIM)

Identifiers

PMID39909217
PMCPMC11875899

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Registered trials

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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.