Evidence map›Paper›PMID 36925557›Full record

ArticleMedComm2023

Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK-IDH2 pathway.

Hao Huang, Shuai Guo, Ya-Qin Chen, Yu-Xing Liu, Jie-Yuan Jin, Yun Liang, Liang-Liang Fan, Rong Xiang

Erratum issuedFull text read
In one paragraph

Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Hao HuangDepartment of Nephrology Xiangya Hospital Central South University Changsha China.ORCID https://orcid.org/0000-0001-9051-4483
Shuai GuoDepartment of Cell Biology School of Life Sciences Central South University Changsha China.
Ya-Qin ChenDepartment of Cardiology Second Xiangya Hospital Central South University Changsha China.
Yu-Xing LiuDepartment of Cell Biology School of Life Sciences Central South University Changsha China.
Jie-Yuan JinDepartment of Cell Biology School of Life Sciences Central South University Changsha China.
Yun LiangDepartment of Cell Biology School of Life Sciences Central South University Changsha China.
Liang-Liang FanDepartment of Nephrology Xiangya Hospital Central South University Changsha China.ORCID https://orcid.org/0000-0001-7431-1838
Rong XiangDepartment of Nephrology Xiangya Hospital Central South University Changsha China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reticulon 3 (RTN3), an endoplasmic reticulum protein, is crucial in neurodegenerative and kidney diseases. However, the role of RTN3 in liver tissues has not been described. Here, we employed public datasets, patients, and several animal models to explore the role of RTN3 in nonalcoholic fatty liver disease (NAFLD). The underlying mechanisms were studied in primary hepatocytes and L02 cells in vitro. We found an increased expression of RTN3 in NAFLD patients, high-fat diet mice, and oxidized low-density lipoprotein-treated L02 cells. The RTN3 transgenic mice exhibited the phenotypes of fatty liver and lipid accumulation. Single-cell RNA sequencing analysis indicated that increased RTN3 might induce mitochondrial dysfunction. We further showed this in primary hepatocytes, the L02 cell line, and the

Indexed as

AMPKIDH2mitochondrial dysfunctionnonalcoholic fatty liver diseaseRTN3

Identifiers

PMID36925557
PMCPMC10013133

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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.