Evidence map›Paper›PMID 25371775›Full record

ReviewOxidative medicine and cellular longevity2014

Nonalcoholic Fatty liver disease: pathogenesis and therapeutics from a mitochondria-centric perspective.

Aaron M Gusdon, Ke-Xiu Song, Shen Qu

Registry-linked trialOpen access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05644717 (Effects of Ertugliflozin on Liver Fat, Liver Fibrosis & Glycemic Control in Subjects With Type 2 Diabetes Mellitus), which is not on this map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
8.4field-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.

NCT05644717 phase4recruitingnot on this mapstarted 2023, after this paper: background citation

Effects of Ertugliflozin on Liver Fat, Liver Fibrosis & Glycemic Control in Subjects With Type 2 Diabetes Mellitus (T2DM) & Non-Alcoholic Fatty Liver Disease /Non-Alcoholic Steatohepatitis

TypeinterventionalSponsorGetz PharmaRan2023 to 2025Enrolled164ConditionsLiver Fat, Liver Fibrosis, Glycemic Control, Body Weight ChangesArmsErtugliflozin 5 mg, 15mg
3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
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  17. Combined Multi-Omics Analysis Reveals the Potential Role ofInternational journal of molecular sciences · 2024
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26 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

3 authors at 3 institutions in 2 countries.

Aaron M GusdonDepartment of Endocrinology and Metabolism, Shanghai 10th People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai 200072, China ; Department of Neurology, Weill Cornell Medical College, New York, NY 10065, USA.
Ke-Xiu SongDepartment of Endocrinology and Metabolism, Shanghai 10th People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai 200072, China.
Shen QuDepartment of Endocrinology and Metabolism, Shanghai 10th People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai 200072, China ; Department of Endocrinology and Metabolism, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Cornell University · USNanjing Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) describes a spectrum of disorders characterized by the accumulation of triglycerides within the liver. The global prevalence of NAFLD has been increasing as the obesity epidemic shows no sign of relenting. Mitochondria play a central role in hepatic lipid metabolism and also are affected by upstream signaling pathways involved in hepatic metabolism. This review will focus on the role of mitochondria in the pathophysiology of NAFLD and touch on some of the therapeutic approaches targeting mitochondria as well as metabolically important signaling pathways. Mitochondria are able to adapt to lipid accumulation in hepatocytes by increasing rates of beta-oxidation; however increased substrate delivery to the mitochondrial electron transport chain (ETC) leads to increased reactive oxygen species (ROS) production and eventually ETC dysfunction. Decreased ETC function combined with increased rates of fatty acid beta-oxidation leads to the accumulation of incomplete products of beta-oxidation, which combined with increased levels of ROS contribute to insulin resistance. Several related signaling pathways, nuclear receptors, and transcription factors also regulate hepatic lipid metabolism, many of which are redox sensitive and regulated by ROS.

Indexed as

AnimalsHumansLipid MetabolismMitochondriaNon-alcoholic Fatty Liver DiseaseReactive Oxygen SpeciesSignal TransductionReactive Oxygen Species

Identifiers

PMID25371775
PMCPMC4211163
OpenAlexW1993016112

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.