Evidence map›Paper›PMID 36509805›Full record

ArticleScientific reports2022

Paraoxonase-2 contributes to promoting lipid metabolism and mitochondrial function via autophagy activation.

Gu-Choul Shin, Hyeong Min Lee, Nayeon Kim, Sang-Ku Yoo, Hyung Soon Park, Leo Sungwong Choi, Kwang Pyo Kim, Ah-Ra Lee, Sang-Uk Seo, Kyun-Hwan Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Paraoxonase 2 as a target for aging-related diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Review
  3. Article
  4. Article
  5. The Paraoxonase (International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. A Case-Control Study Supports Genetic Contribution of theAntioxidants (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Açaí (Nutrients · 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

10 authors at 5 institutions in 1 country.

Gu-Choul Shin *Department of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Hyeong Min Lee *Department of Applied Chemistry, Institute of Natural Science, Global Center for Pharmaceutical Ingredient Materials, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Nayeon KimDepartment of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Sang-Ku YooGlaceum Inc., Suwon, Republic of Korea.
Hyung Soon ParkGlaceum Inc., Suwon, Republic of Korea.
Leo Sungwong ChoiGlaceum Inc., Suwon, Republic of Korea.
Kwang Pyo KimDepartment of Applied Chemistry, Institute of Natural Science, Global Center for Pharmaceutical Ingredient Materials, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Ah-Ra LeeDepartment of Microbiology College of Medicine, Songeui Medical Campus, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Sang-Uk SeoDepartment of Microbiology College of Medicine, Songeui Medical Campus, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Kyun-Hwan KimDepartment of Precision Medicine, School of Medicine, Sungkyunkwan University, Suwon, 16419, Republic of Korea. khkim10@skku.edu.
Catholic University of Korea · KRGlaceum (South Korea) · KRKyung Hee University Medical Center · KRKyung Hee University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent immuno-metabolic disease that can progress to hepatic cirrhosis and cancer. NAFLD pathogenesis is extremely complex and is characterized by oxidative stress, impaired mitochondrial function and lipid metabolism, and cellular inflammation. Thus, in-depth research on its underlying mechanisms and subsequent investigation into a potential drug target that has overarching effects on these features will help in the discovery of effective treatments for NAFLD. Our study examines the role of endogenous paraoxonase-2 (PON2), a membrane protein with reported antioxidant activity, in an in vitro cell model of NAFLD. We found that the hepatic loss of PON2 activity aggravated steatosis and oxidative stress under lipotoxic conditions, and our transcriptome analysis revealed that the loss of PON2 disrupts the activation of numerous functional pathways closely related to NAFLD pathogenesis, including mitochondrial respiratory capacity, lipid metabolism, and hepatic fibrosis and inflammation. We found that PON2 promoted the activation of the autophagy pathway, specifically the mitophagy cargo sequestration, which could potentially aid PON2 in alleviating oxidative stress, mitochondrial dysfunction, lipid accumulation, and inflammation. These results provide a mechanistic foundation for the prospect of PON2 as a drug target, leading to the development of novel therapeutics for NAFLD.

Indexed as

Lipid MetabolismNon-alcoholic Fatty Liver DiseaseAutophagyHumansInflammationLiverMitochondriaOxidative Stress

Identifiers

PMID36509805
PMCPMC9744871
OpenAlexW4311222814

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.