Evidence map›Paper›PMID 12631701›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Functional proteomics of nonalcoholic steatohepatitis: mitochondrial proteins as targets of S-adenosylmethionine.

Enrique Santamaria, Matías A Avila, M Ujue Latasa, Angel Rubio, Antonio Martin-Duce, Shelly C Lu, José M Mato, Fernando J Corrales

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.6field-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

61 citing papers in PubMed, 164 citations in OpenAlex.

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  18. Prohibitin 1 in liver injury and cancer.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  19. Article
  20. Methionine adenosyltransferases in liver cancer.World journal of gastroenterology · 2019
    Review

1 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

8 authors at 1 institution in 1 country.

Enrique SantamariaLaboratorio de Proteómica, Genómica y Bioinformática, and División de Hepatologia y Terapia Génica, Facultad de Medicina, Universidad de Navarra, 31008 Pamplona, Spain.
Matías A Avila
M Ujue Latasa
Angel Rubio
Antonio Martin-Duce
Shelly C Lu
José M Mato
Fernando J Corrales
Universidad de Navarra · ES

Funding

Role of SAMe in Pathogenesis and Treatment of Non-Alcholic Fatty Liver DiseaseR01AT001576 · NCCIH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2002 to 2018
$5.0M
REGULATION OF S-ADENOSYLMETHIONINE SYNTHETASE IN LIVERR01DK051719 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 1997 to 2014
$4.5M
ALTERED METHIONINE METABOLISM IN ALCOHOLIC LIVER INJURYR01AA012677 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2001 to 2005
$1.9M
MAT1A NULL MOUSE: MODEL FOR ALCOHOLIC TISSUE INJURYR01AA013847 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2003 to 2007
$1.8M
NCCIH NIH HHS R01 AT001576NCCIH NIH HHS R01 AT 1576NIAAA NIH HHS R01 AA012677NIAAA NIH HHS R01 AA013847NIAAA NIH HHS R01 AA 12677NIAAA NIH HHS R01 AA 13847NIDDK NIH HHS R01 DK051719NIDDK NIH HHS R01 DK 51719
6 · The paper itself

Abstract

Recent work shows that S-adenosylmethionine (AdoMet) helps maintain normal liver function as chronic hepatic deficiency results in spontaneous development of steatohepatitis and hepatocellular carcinoma. The mechanisms by which these nontraditional functions of AdoMet occur are unknown. Here, we use knockout mice deficient in hepatic AdoMet synthesis (MAT1A(-/-)) to study the proteome of the liver during the development of steatohepatitis. One hundred and seventeen protein spots, differentially expressed during the development of steatohepatitis, were selected and identified by peptide mass fingerprinting. Among them, 12 proteins were found to be affected from birth, when MAT1A(-/-) expression is switched on in WT mouse liver, to the rise of histological lesions, which occurs at approximately 8 months. Of the 12 proteins, 4 [prohibitin 1 (PHB1), cytochrome c oxidase I and II, and ATPase beta-subunit] have known roles in mitochondrial function. We show that the alteration in expression of PHB1 correlates with a loss of mitochondrial function. Experiments in isolated rat hepatocytes indicate that AdoMet regulates PHB1 content, thus suggesting ways by which steatohepatitis may be induced. Importantly, we found the expression of these mitochondrial proteins was abnormal in obob mice and obese patients who are at risk for nonalcoholic steatohepatitis.

Indexed as

Repressor ProteinsAnimalsElectron Transport Complex IVHepatitisHumansIn Vitro TechniquesIsoenzymesMethionine AdenosyltransferaseMiceMice, KnockoutMice, ObeseMitochondrial ProteinsObesityPeptide MappingProhibitinsProteinsElectron Transport Complex IVIsoenzymesMethionine AdenosyltransferaseMitochondrial ProteinsPHB protein, humanProhibitinsProteinsRepressor ProteinsRNA, MessengerS-Adenosylmethionine

Identifiers

PMID12631701
PMCPMC152247
OpenAlexW2068264995

What OpenQuestion holds

Textmetadata
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.