Evidence map›Paper›PMID 32520409›Full record

ArticleBritish journal of pharmacology2020

Sirtuin 3-mediated deacetylation of acyl-CoA synthetase family member 3 by protocatechuic acid attenuates non-alcoholic fatty liver disease.

Ruimin Sun, Xiaohui Kang, Yan Zhao, Zhanyu Wang, Ruiwen Wang, Rong Fu, Yang Li, Yan Hu, Zhecheng Wang, Wen Shan and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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  20. Histone Modifications in NAFLD: Mechanisms and Potential Therapy.International journal of molecular sciences · 2023
    Review
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

13 authors at 1 institution in 1 country.

Ruimin SunDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Xiaohui KangDepartment of Pharmacy, Dalian Medical University, Dalian, China.
Yan ZhaoDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Zhanyu WangDepartment of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Ruiwen WangDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Rong FuDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Yang LiDepartment of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Yan HuDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Zhecheng WangDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Wen ShanDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Junjun ZhouDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Xiaofeng TianDepartment of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Jihong YaoDepartment of Pharmacology, Dalian Medical University, Dalian, China.ORCID 0000-0001-5940-9167
Dalian Medical University · CN

Funding

Doctoral Scientific Research Foundation of Liaoning Province China 20180540038National Natural Science Foundation of China 21704011National Natural Science Foundation of China 81603369National Natural Science Foundation of China 81703771National Natural Science Foundation of China 81773799
6 · The paper itself

Abstract

background and purposeHepatic fatty acid metabolism disorder, a key pathogenic mechanism underlying non-alcoholic fatty liver disease (NAFLD), is associated with the hyperacetylation of mitochondrial enzymes. Acyl-CoA synthetase family member 3 (ACSF3), which is involved in the regulation of fatty acid metabolism, was predicted to contain lysine acetylation sites related to the mitochondrial deacetylase sirtuin 3 (SIRT3). The purpose of this study was to explore the underlying mechanism by which SIRT3 deacetylates ACSF3 in NAFLD and the protective effect of the natural phenolic compound protocatechuic acid (PCA) against fatty acid metabolism disorder via the SIRT3/ACSF3 pathway. EXPERIMENTAL APPROACH: The role of protocatechuic acid and its molecular mechanism in NAFLD were detected in rats and SIRT3-knockout mice fed a high-fat diet (HFD) and in AML-12 cells treated with palmitic acid (PA). KEY

resultsPharmacological treatment with protocatechuic acid significantly attenuated high-fat diet-induced fatty acid metabolism disorder in NAFLD. Molecular docking assays showed that protocatechuic acid specifically bound SIRT3 as a substrate and increased SIRT3 protein expression. However, the protective role of protocatechuic acid was abolished by SIRT3 knockdown, which increased ACSF3 expression and exacerbated fatty acid metabolism disorder. Mechanistically, SIRT3 was shown to specifically regulate the acetylation and degradation of ACSF3, which govern the capacity of ACSF3 to mediate fatty acid metabolism disorder during NAFLD. CONCLUSION AND IMPLICATIONS: SIRT3-mediated ACSF3 deacetylation is a novel molecular mechanism in NAFLD therapy and protocatechuic acid confers protection against high-fat diet- and palmitic acid-induced hepatic fatty acid metabolism disorder through the SIRT3/ACSF3 pathway.

Indexed as

HydroxybenzoatesNon-alcoholic Fatty Liver DiseaseSirtuin 3AnimalsCoenzyme ADiet, High-FatLigasesLiverMiceMolecular Docking SimulationRatsCoenzyme AHydroxybenzoatesLigasesprotocatechuic acidSirtuin 3ACSF3fatty acid metabolismNAFLDprotocatechuic acidSIRT3

Identifiers

PMID32520409
PMCPMC7443473
OpenAlexW3032896625

What Socratic 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 Socratic graph.