Evidence map›Paper›PMID 23123815›Full record

ReviewBiochimica et biophysica acta2013

Mitochondrial glutathione: features, regulation and role in disease.

Montserrat Marí, Albert Morales, Anna Colell, Carmen García-Ruiz, Neil Kaplowitz, José C Fernández-Checa

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 199 citations in OpenAlex.

  1. Pooled it
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  15. Isa2p is essential inJournal of biosciences · 2025
    Article
  16. Control of mitochondrial glutathione homeostasis by SLC25A39.Acta biochimica et biophysica Sinica · 2024
    Article
  17. Review
  18. Article
  19. Review
  20. Article

37 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Montserrat MaríDepartment of Cell Death and Proliferation, IIBB-CSIC, Barcelona, Spain. monmari@clinic.ub.es
Albert Morales
Anna Colell
Carmen García-Ruiz
Neil Kaplowitz
José C Fernández-Checa
Centro de Investigación Biomédica en Red · ESInstitut d'Investigacions Biomèdiques de Barcelona · ESUniversity of Southern California · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
Homocysteine, ER Stress and Alcoholic Liver Injury.R01AA014428 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JI, CHENG, KAPLOWITZ, NEIL · 2004 to 2014
$3.7M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS R01 AA014428NIDDK NIH HHS P30 DK048522
6 · The paper itself

Abstract

backgroundMitochondria are the powerhouse of mammalian cells and the main source of reactive oxygen species (ROS) associated with oxygen consumption. In addition, they also play a strategic role in controlling the fate of cells through regulation of death pathways. Mitochondrial ROS production fulfills a signaling role through regulation of redox pathways, but also contributes to mitochondrial damage in a number of pathological states. SCOPE OF REVIEW: Mitochondria are exposed to the constant generation of oxidant species, and yet the organelle remains functional due to the existence of an armamentarium of antioxidant defense systems aimed to repair oxidative damage, of which mitochondrial glutathione (mGSH) is of particular relevance. Thus, the aim of the review is to cover the regulation of mGSH and its role in disease. MAJOR

conclusionsCumulating evidence over recent years has demonstrated the essential role for mGSH in mitochondrial physiology and disease. Despite its high concentration in the mitochondrial matrix, mitochondria lack the enzymes to synthesize GSH de novo, so that mGSH originates from cytosolic GSH via transport through specific mitochondrial carriers, which exhibit sensitivity to membrane dynamics. Depletion of mGSH sensitizes cells to stimuli leading to oxidative stress such as TNF, hypoxia or amyloid β-peptide, thereby contributing to disease pathogenesis. GENERAL SIGNIFICANCE: Understanding the regulation of mGSH may provide novel insights to disease pathogenesis and toxicity and the opportunity to design therapeutic targets of intervention in cell death susceptibility and disease. This article is part of a Special Issue entitled Cellular functions of glutathione.

Indexed as

AnimalsAntioxidantsBiological TransportCytosolGlutathioneHumansMitochondriaOxidative StressAntioxidantsGlutathione

Identifiers

PMID23123815
PMCPMC3578987
OpenAlexW2018427017

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.