Evidence map›Paper›PMID 39828951›Full record

ArticleGlia2025

Acute Extrinsic Activation of the RANKL Pathway Decreases Wound Healing and Functional Recovery After Spinal Cord Injury in Mice.

A L Vivinetto, A Bernstein, M Soliman, J W Cave, E Hollis

Abstract read
In one paragraph

Article in Glia, 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

5 authors.

A L VivinettoBurke Neurological Institute, White Plains, New York, USA.ORCID 0000-0001-5054-6974
A BernsteinBurke Neurological Institute, White Plains, New York, USA.ORCID 0000-0002-6619-4878
M SolimanBurke Neurological Institute, White Plains, New York, USA.ORCID 0000-0001-7118-4546
J W CaveIn Vitro Cell Research LLC, Fort Lee, New Jersey, USA.ORCID 0000-0003-1792-7219
E HollisBurke Neurological Institute, White Plains, New York, USA.ORCID 0000-0002-4535-4668

Funding

Modulation of cortical networks, a new approach to spinal cord injury rehabilitationDP2NS106663 · NINDS · WINIFRED MASTERSON BURKE MED RES INST · PI HOLLIS, EDMUND R · 2017 to 2020
$2.8M
Advanced, multi-function, inverted confocal microscope for BNI Structural and Functional Imaging CoreS10OD028547 · OD · WINIFRED MASTERSON BURKE MED RES INST · PI HOLLIS, EDMUND R · 2020 to 2020
$530k
Craig H. Neilsen Foundation 649532New York State Department of Health C37717GGNIH HHS DP2 NS106663NIH HHS S10 OD028547NINDS NIH HHS DP2 NS106663
6 · The paper itself

Abstract

Manipulating wound healing-associated signaling after SCI presents a promising avenue for increasing the recovery of function after injury. This study explores the potential of targeting molecular regulators of wound healing, initially identified in nonneural tissues, to enhance outcomes after SCI. Astrocytes, pivotal in central nervous system wound healing, play a crucial role in tissue remodeling and recovery. However, the optimal manipulation of astrogliosis for beneficial outcomes remains elusive. Previous research demonstrated a transcriptional response in astrocytes resembling epithelial-to-mesenchymal transitions (EMTs) after CNS injury. Here, we investigate the extrinsic manipulation of wound healing through the Receptor Activator of Nuclear-factor Kappa-Β (RANK) pathway, known for its involvement in nonneural tissue remodeling and linked to EMT pathway. Using a severe thoracic spinal cord contusion mouse model, we demonstrate that acute activation of the RANK pathway with RANK ligand (RANKL) adversely affects tissue remodeling, resulting in larger lesion volumes and delayed recovery of posture and locomotion. These findings suggest that early perturbations in the tight molecular regulation of tissue remodeling negatively impact the wound-healing process after SCI. The study provides a proof-of-concept demonstration that exogenous nonneural remodeling ligands can modify astrocyte responses and functional recovery after SCI, raising questions about the optimal time frame for beneficial remodeling interventions during injury progression. These insights open new avenues for therapeutic strategies aimed at improving functional outcomes following SCI.

Indexed as

RANK LigandRecovery of FunctionSignal TransductionSpinal Cord InjuriesWound HealingAnimalsAstrocytesDisease Models, AnimalFemaleMiceMice, Inbred C57BLRANK LigandTnfsf11 protein, mouse

Identifiers

PMID39828951
PMCPMC11922651

What Socratic 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 Socratic graph.