Evidence map›Paper›PMID 18956292›Full record

ReviewSeminars in liver disease2008

Molecular mechanisms of lipotoxicity in nonalcoholic fatty liver disease.

Harmeet Malhi, Gregory J Gores

Abstract readReview
In one paragraph

Review in Seminars in liver disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 papers.

0numbers the graph read from it
0cells of the map it votes in
270citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

270 citing papers in PubMed, 538 citations in OpenAlex.

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210 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

2 authors at 1 institution in 1 country.

Harmeet MalhiMiles and Shirley Fiterman Center for Digestive Diseases, Mayo Clinic, College of Medicine, Rochester, Minnesota 55905, USA.
Gregory J Gores
Mayo Clinic in Arizona · US

Funding

MECHANISMS OF LIVER CELL INJURYR01DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 1992 to 2019
$3.6M
MECHANISMS OF LIVER CELL INJURYR37DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2000 to 2009
$2.9M
INTRACELLULAR PH IN LIVER CELL INJURYR29DK041876 · NIDDK · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GORES, GREGORY J. · 1989 to 1992
–
NIDDK NIH HHS DK41876NIDDK NIH HHS R01 DK041876NIDDK NIH HHS R37 DK041876
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is characterized by insulin resistance, which results in elevated serum concentration of free fatty acids (FFAs). Circulating FFAs provide the substrate for triacylglycerol formation in the liver, and may also be directly cytotoxic. Hepatocyte apoptosis is a key histologic feature of NAFLD, and correlates with progressive inflammation and fibrosis. The molecular pathways leading to hepatocyte apoptosis are not fully defined; however, recent studies suggest that FFA-induced apoptosis contributes to the pathogenesis of nonalcoholic steatohepatitis. FFAs directly engage the core apoptotic machinery by activating the proapoptotic protein Bax, in a c-jun N-terminal kinase-dependent manner. FFAs also activate the lysosomal pathway of cell death and regulate death receptor gene expression. The role of ER stress and oxidative stress in the pathogenesis of nonalcoholic steatohepatitis has also been described. Understanding the molecular mediators of liver injury should promote development of mechanism-based therapeutic interventions.

Indexed as

ApoptosisEndoplasmic ReticulumFatty Acids, NonesterifiedFatty LiverHepatocytesHumansJNK Mitogen-Activated Protein KinasesLiverMitochondria, LiverToll-Like ReceptorsTumor Necrosis Factor-alphaFatty Acids, NonesterifiedJNK Mitogen-Activated Protein KinasesToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID18956292
PMCPMC2908270
OpenAlexW2067038570

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.