Evidence map›Paper›PMID 31102563›Full record

ArticleNeurourology and urodynamics2019

Acute spinal cord injury is associated with mitochondrial dysfunction in mouse urothelium.

Aura F Kullmann, Steven T Truschel, Amanda S Wolf-Johnston, Bronagh M McDonnell, A M Lynn, Anthony John Kanai, Thomas M Kessler, Gerard Apodaca, Lori A Birder

Abstract read
In one paragraph

Article in Neurourology and urodynamics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 9% of its field
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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  8. Targeted Mitochondrial Delivery to Hepatocytes: A Review.Journal of clinical and translational hepatology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Aura F KullmannDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Steven T TruschelDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Amanda S Wolf-JohnstonDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Bronagh M McDonnellDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
A M LynnDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Anthony John KanaiDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Thomas M KesslerDepartment of Neuro-Urology, Balgrist University Hospital, University of Zürich, Zürich, Switzerland.
Gerard ApodacaDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Lori A BirderDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
University of Pittsburgh · USUniversity of Zurich · CH

Funding

Urothelium in Detrusor OveractivityP01DK093424 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KANAI, ANTHONY JOHN · 2013 to 2017
$7.9M
JEOL JEM-1011 TRANSMISSION ELECTRON MICROSCOPE: MUSCULAR DYSTROPHYS10RR019003 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WATKINS, SIMON C · 2004 to 2004
$337k
NCRR NIH HHS S10 RR019003NIDDK NIH HHS P01 DK093424
6 · The paper itself

Abstract

aimTo characterize the effects of acute spinal cord injury (SCI) on mitochondrial morphology and function in bladder urothelium and to test the therapeutic efficacy of early treatment with the mitochondrially targeted antioxidant, MitoTempo.

methodsWe used a mouse model of acute SCI by spinal cord transection between the T8-T9 vertebrae with or without MitoTempo delivery at the time of injury followed by tissue processing at 3 days after SCI. Control, SCI, and SCI-MitoTempo-treated mice were compared in all experimental conditions. Assessments included analysis of markers of mitochondrial health including accumulation of reactive oxygen species (ROS), morphological changes in the ultrastructure of mitochondria by transmission electron microscopy, and Western blot analysis to quantify protein levels of markers for autophagy and altered mitochondrial dynamics.

resultsSCI resulted in an increase in oxidative stress markers and ROS production, confirming mitochondrial dysfunction. Mitochondria from SCI mice developed large electron-dense inclusions and these aberrant mitochondria accumulated throughout the cytoplasm suggesting an inability to clear dysfunctional mitochondria by mitophagy. SCI mice also exhibited elevated levels of dynamin-related protein 1 (DRP1), consistent with a disruption of mitochondrial dynamics. Remarkably, treatment with MitoTempo reversed many of the SCI-induced abnormalities that we observed.

conclusionsAcute SCI negatively and severely affects mitochondrial health of bladder urothelium. Early treatment of SCI with MitoTempo may be a viable therapeutic agent to mitigate these deleterious effects.

Indexed as

Acute DiseaseAnimalsAntioxidantsApoptosisAutophagyDynaminsFemaleMiceMice, Inbred C57BLMitochondriaMitochondrial DiseasesOrganophosphorus CompoundsOxidative StressPiperidinesReactive Oxygen SpeciesSpinal Cord InjuriesAntioxidantsDnm1l protein, mouseDynaminsMitoTEMPOOrganophosphorus CompoundsPiperidinesReactive Oxygen Speciesbladdermitochondrial membrane potentialROS

Identifiers

PMID31102563
PMCPMC7528977
OpenAlexW2945412633

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.