Evidence map›Paper›PMID 28888203›Full record

ArticleRedox biology2018

Role of glutathione biosynthesis in endothelial dysfunction and fibrosis.

Cristina Espinosa-Díez, Verónica Miguel, Susana Vallejo, Francisco J Sánchez, Elena Sandoval, Eva Blanco, Pablo Cannata, Concepción Peiró, Carlos F Sánchez-Ferrer, Santiago Lamas

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Contrasting the genetic architecture of cardiac glutathione against other organs: unveiling a unique tissue-specific locus.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  19. Enhancing Bioactive Components ofAntioxidants (Basel, Switzerland) · 2022
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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

10 authors at 3 institutions in 1 country.

Cristina Espinosa-DíezDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain.
Verónica MiguelDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain.
Susana VallejoDepartment of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Spain.
Francisco J SánchezDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain.
Elena SandovalDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain.
Eva BlancoDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain.
Pablo CannataDepartment of Pathology, Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Spain.
Concepción PeiróDepartment of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Spain.
Carlos F Sánchez-FerrerDepartment of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Spain.
Santiago LamasDepartment of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa", (CSIC-UAM), Madrid, Spain. Electronic address: slamas@cbm.csic.es.
Universidad Autónoma de Madrid · ESHospital Universitario La Paz · ESCentro de Biología Molecular Severo Ochoa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutathione (GSH) biosynthesis is essential for cellular redox homeostasis and antioxidant defense. The rate-limiting step requires glutamate-cysteine ligase (GCL), which is composed of the catalytic (GCLc) and the modulatory (GCLm) subunits. To evaluate the contribution of GCLc to endothelial function we generated an endothelial-specific Gclc haplo-insufficient mouse model (Gclc e/+ mice). In murine lung endothelial cells (MLEC) derived from these mice we observed a 50% reduction in GCLc levels compared to lung fibroblasts from the same mice. MLEC obtained from haplo-insufficient mice showed significant reduction in GSH levels as well as increased basal and stimulated ROS levels, reduced phosphorylation of eNOS (Ser 1177) and increased eNOS S-glutathionylation, compared to MLEC from wild type (WT) mice. Studies in mesenteric arteries demonstrated impaired endothelium-dependent vasodilation in Gclc(e/+) male mice, which was corrected by pre-incubation with GSH-ethyl-ester and BH

Indexed as

AnimalsBiopterinsCells, CulturedDisease Models, AnimalEndothelial CellsFemaleFibroblastsFibrosisGlutamate-Cysteine LigaseGlutathioneHaploinsufficiencyKidneyKidney DiseasesMaleMesenteric ArteriesMiceBiopterinsGlutamate-Cysteine LigaseGlutathioneNitric Oxide Synthase Type IIIReactive Oxygen SpeciessapropterinEndothelial dysfunctionGlutamate-cysteine ligaseGlutathioneKidney FibrosisROS

Identifiers

PMID28888203
PMCPMC5596265
OpenAlexW3024748658

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.