Evidence map›Paper›PMID 38510106›Full record

ArticleFrontiers in cellular neuroscience2024

5-HT

Natalie E Scholpa, Epiphani C Simmons, Austin D Thompson, Seth S Carroll, Rick G Schnellmann

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.0field-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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Journal of tissue engineering
    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 at 2 institutions in 1 country.

Natalie E Scholpa *Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States.
Epiphani C Simmons *Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States.
Austin D ThompsonDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States.
Seth S CarrollDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States.
Rick G SchnellmannDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, United States.
University of Arizona · USArizona Science Center · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
5-HT1F receptor mediated mitochondrial biogenesis for the treatment of spinal cord injuryF31NS115413 · NINDS · UNIVERSITY OF ARIZONA · PI SIMMONS, EPIPHANI · 2020 to 2020
$37k
5-HT1F receptor agonism as a novel therapeutic strategy following spinal cord injuryI01BX004868 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI SCHNELLMANN, RICK G · 2020 to 2023
–
The Role of Epigenetics in Mitochondrial Biogenesis-Mediated Recovery after Spinal Cord InjuryIK2BX005218 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI SCHOLPA, NATALIE E · 2020 to 2024
–
BLRD VA I01 BX004868BLRD VA IK2 BX005218NIEHS NIH HHS P30 ES006694NIEHS NIH HHS T32 ES007091NINDS NIH HHS F31 NS115413
6 · The paper itself

Abstract

Introduction: Vascular and mitochondrial dysfunction are well-established consequences of multiple central nervous system (CNS) disorders, including neurodegenerative diseases and traumatic injuries. We previously reported that 5-hydroxytryptamine 1F receptor (5-HT Methods: Lasmiditan is a selective 5-HT Results: Lasmiditan treatment increased the maximal oxygen consumption rate, mitochondrial proteins and mitochondrial density in mBMEC, indicative of MB induction. Lasmiditan also enhanced endothelial cell migration and tube formation, key components of angiogenesis. Trans-endothelial electrical resistance (TEER) and tight junction protein expression, including claudin-5, were also increased with lasmiditan, suggesting improved barrier function. Finally, lasmiditan treatment decreased phosphorylated VE-Cadherin and induced activation of the Akt-FoxO1 pathway, which decreases FoxO1-mediated inhibition of claudin-5 transcription. Discussion: These data demonstrate that lasmiditan induces MB and enhances endothelial cell function, likely via the VE-Cadherin-Akt-FoxO1-claudin-5 signaling axis. Given the importance of mitochondrial and vascular dysfunction in neuropathologies, 5-HT

Indexed as

5-HT1F receptorblood–brain barrierblood–spinal cord barrierendothelial cellslasmiditanmitochondrial biogenesisvascular recovery

Identifiers

PMID38510106
PMCPMC10952819
OpenAlexW4392468446

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.