Evidence mapPaperPMID 34794886Full record

ArticleInternational immunopharmacology2021

P53 mediates the protective effects of metformin in inflamed lung endothelial cells.

Khadeja-Tul Kubra, Mohammad A Uddin, Mohammad S Akhter, Antoinette J Leo, Agnieszka Siejka, Nektarios Barabutis

Open access · greenAbstract read
In one paragraph

Article in International immunopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025
    Review
  2. Unfolded protein response in endothelial injury.Cell cycle (Georgetown, Tex.) · 2022
    Article
  3. Review
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

6 authors at 2 institutions in 2 countries.

Khadeja-Tul KubraSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA.
Mohammad A UddinSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA.
Mohammad S AkhterSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA.
Antoinette J LeoSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA.
Agnieszka SiejkaDepartment of Clinical Endocrinology, Medical University of Lodz, Lodz, Poland.
Nektarios BarabutisSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA. Electronic address: barabutis@ulm.edu.
University of Louisiana at Monroe · USMedical University of Lodz · PL

Funding

Molecular and Cell Biology Resources CoreP20GM103424 · LOUISIANA STATE UNIV A&M COL BATON ROUGE · 2025 to 2025
$4.1M
NIGMS NIH HHS P20 GM103424
6 · The paper itself

Abstract

The endothelial barrier regulates interstitial fluid homeostasis by transcellular and paracellular means. Dysregulation of this semipermeable barrier may lead to vascular leakage, edema, and accumulation of pro-inflammatory cytokines, inducing microvascular hyperpermeability. Investigating the molecular pathways involved in those events will most probably provide novel therapeutic possibilities in pathologies related to endothelial barrier dysfunction. Metformin (MET) is an anti-diabetic drug, opposes malignancies, inhibits cellular transformation, and promotes cardiovascular protection. In the current study, we assess the protective effects of MET in LPS-induced lung endothelial barrier dysfunction and evaluate the role of P53 in mediating the beneficial effects of MET in the vasculature. We revealed that this biguanide (MET) opposes the LPS-induced dysregulation of the lung microvasculature, since it suppressed the formation of filamentous actin stress fibers, and deactivated cofilin. To investigate whether P53 is involved in those phenomena, we employed the fluorescein isothiocyanate (FITC) - dextran permeability assay, to measure paracellular permeability. Our observations suggest that P53 inhibition increases paracellular permeability, and MET prevents those effects. Our results contribute towards the understanding of the lung endothelium and reveal the significant role of P53 in the MET-induced barrier enhancement.

Indexed as

AnimalsCardiac MyosinsCattleEndothelial CellsGene Expression RegulationHypoglycemic AgentsInflammationLipopolysaccharidesMetforminMyosin Light ChainsPulmonary ArteryTumor Suppressor Protein p53Cardiac MyosinsHypoglycemic AgentsLipopolysaccharidesMetforminmyosin light chain 2Myosin Light ChainsTumor Suppressor Protein p53EndotheliumHyperpermeabilityInflammationVascular barrierVasculature

Identifiers

PMID34794886
PMCPMC8678340
OpenAlexW3211837180

What Socratic 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 Socratic graph.