Evidence map›Paper›PMID 36386234›Full record

ArticleFrontiers in pharmacology2022

BCATc inhibitor 2 ameliorated mitochondrial dysfunction and apoptosis in oleic acid-induced non-alcoholic fatty liver disease model.

Zhuo Lu, Gui-Feng Sun, Xiao-An Pan, Xin-Hui Qu, Ping Yang, Zhi-Ping Chen, Xiao-Jian Han, Tao Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Exploring Cirrhosis: Insights into Advances in Therapeutic Strategies.International journal of molecular sciences · 2025
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  12. Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023
    Review
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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

8 authors at 3 institutions in 1 country.

Zhuo LuInstitute of Geriatrics, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Gui-Feng SunDepartment of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang, China.
Xiao-An PanDepartment of Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang, China.
Xin-Hui QuInstitute of Geriatrics, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Ping YangDepartment of Neurology, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Zhi-Ping ChenDepartment of Critical Care Medicine, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Xiao-Jian HanInstitute of Geriatrics, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Tao WangInstitute of Geriatrics, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
First Affiliated Hospital of Jiangxi Medical College · CNJiangxi Provincial People's Hospital · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a prevalent hepatic disease in the world. Disorders of branched chain amino acid (BCAA) metabolism is involved in various diseases. In this study, we aim to explore the role of BCAA metabolism in the development of NAFLD and the protective effect of BCATc Inhibitor 2, an inhibitor of cytosolic branched chain amino acid transaminase, against NAFLD as well as its underlying mechanism. It was found that oleic acid induced lipid accumulation and apoptosis in HepG2 and LO2 cells. Supplementation of BCAAs further aggravated oleic acid-induced lipid accumulation and apoptosis. In contrast, treatment of BCATc Inhibitor 2 ameliorated oleic acid-induced lipid accumulation and apoptosis. Molecularly, supplementation of BCAAs or treatment of BCATc Inhibitor 2 up-regulated or down-regulated the expression of SREBP1 and lipogenesis-related genes without affecting lipolysis-related genes. BCATc Inhibitor 2 maintained mitochondrial function by ameliorating oleic acid-induced mitochondrial ROS generation and mitochondrial membrane potential disruption. In addition, BCATc Inhibitor 2 treatment alleviated oleic acid-induced activation of JNK and AKT signaling pathway and Bcl2/Bax/Caspase axis. In conclusion, our results indicate BCAA metabolism is involved in NAFLD and BCATc Inhibitor 2 protects against oleic acid-induced lipid accumulation and apoptosis. These findings suggest that BCATc Inhibitor 2 is a promising candidate drug for the treatment of NAFLD.

Indexed as

apoptosisBCTAc inhibitor 2mitochondrial dysfunctionNAFLDoxidative stress

Identifiers

PMID36386234
PMCPMC9650408
OpenAlexW4307460116

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.