Evidence map›Paper›PMID 37026514›Full record

ArticleInternational journal of molecular medicine2023

Overexpression of salusin‑α upregulates AdipoR2 and activates the PPARα/ApoA5/SREBP‑1c pathway to inhibit lipid synthesis in HepG2 cells.

Huan Zhang, Chao Yang, Songjiao Wang, Aohong Xu, Qian Zhang, Xiuqun Duan, Guofu Gong, Yuxue Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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.

Huan Zhang *Department of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.
Chao Yang *Department of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.
Songjiao WangDepartment of Clinical Laboratory, Ezhou Central Hospital, Ezhou, Hubei 436000, P.R. China.
Aohong XuDepartment of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.
Qian ZhangDepartment of Emergency, Xiangyang Central Hospital, Xiangyang, Hubei 441032, P.R. China.
Xiuqun DuanDepartment of Clinical Laboratory, Ezhou Central Hospital, Ezhou, Hubei 436000, P.R. China.
Guofu Gong *Department of Clinical Laboratory, Ezhou Central Hospital, Ezhou, Hubei 436000, P.R. China.
Yuxue Wang *Department of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.
Hubei University of Chinese Medicine · CNEzhou Central Hospital · CNXiangyang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Salusin‑α and adiponectin, are vasoactive peptides with numerous similar biological effects related to lipid metabolism. Adiponectin has been shown to reduce fatty acid oxidation and to inhibit lipid synthesis of liver cells through its receptor, adiponectin receptor 2 (AdipoR2), but whether salusin‑α is able to interact with AdipoR2, was not previously reported. To investigate this,

Indexed as

AdiponectinPPAR alphaApolipoprotein A-VHep G2 CellsHumansLipid MetabolismSterol Regulatory Element Binding Protein 1ThapsigarginAdiponectinApolipoprotein A-VPPAR alphaSterol Regulatory Element Binding Protein 1Thapsigarginadiponectin receptor 2lentiviruslipid metabolismPPARα/ApoA5/SREBP‑1c axissalusin‑α

Identifiers

PMID37026514
PMCPMC10094946
OpenAlexW4362669851

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.