Evidence map›Paper›PMID 35590369›Full record

ArticleJournal of translational medicine2022

SORBS2 as a molecular target for atherosclerosis in patients with familial hypercholesterolemia.

Ming-Ming Liu, Jia Peng, Yuan-Lin Guo, Cheng-Gang Zhu, Na-Qiong Wu, Rui-Xia Xu, Qian Dong, Chuan-Jue Cui, Jian-Jun Li

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Observational
  5. Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025
    Review
  6. Article
  7. Article
  8. Lymphangiogenesis: A new strategy for heart disease treatment (Review).International journal of molecular medicine · 2024
    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

9 authors at 1 institution in 1 country.

Ming-Ming LiuCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Jia PengCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Yuan-Lin GuoCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Cheng-Gang ZhuCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Na-Qiong WuCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Rui-Xia XuCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Qian DongCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China.
Chuan-Jue CuiCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China. cuichuanjue@fuwaihospital.org.
Jian-Jun LiCardiovascular Metabolic Center, State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 BeiLiShi Road, XiCheng District, Beijing, China. lijianjun938@126.com.ORCID 0000-0003-2536-4364
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFamilial hypercholesterolemia (FH) is a metabolic disease in which patients are prone to develop premature atherosclerosis (AS). Sorbin and SH3 Domain Containing 2 (SORBS2) is known to play a role in coronary heart disease (CHD). However, the mechanism underlying SORBS2 involvement in the development of hypercholesterolemia remains unknown. Here, we investigated the effects of SORBS2 on inflammation and foam cell formation and its underlying mechanisms.

methodsUsing Bioinformatics analysis, we established that SORBS2 is upregulated in patients with FH. Circulating concentrations of SORBS2 were measured using ELISA kit (n = 30). The association between circulating SORBS2 levels and inflammatory factors or lipid indexes were conducted using Spearman correlation analysis. We further conducted in vitro experiments that the expression of SORBS2 were analyzed, and SORBS2 siRNA were transfected into oxidized LDL (OxLDL)-induced macrophages, followed by western blot and immunofluorescence.

resultsCirculating SORBS2 levels were positively associated with inflammatory factors and lipid indexes. We also observed that high in vitro expression of SORBS2 in OxLDL-induced macrophages. After SORBS2 silencing, Nod like receptor family pyrin domain-containing 3 protein(NLRP3)-Caspase1 activation and NF-κB activation were attenuated, and secretion of pro-inflammatory cytokines (IL-1β and IL-18) was decreased. Moreover, SORBS2 silencing blocked reactive oxygen species (ROS) production and lipid accumulation, and promoted cholesterol efflux through ABCG1-PPARγ pathway.

conclusionsSORBS2 regulates lipid-induced inflammation and foam cell formation, and is a potential therapeutic target for hypercholesterolemia.

Indexed as

AtherosclerosisHypercholesterolemiaHyperlipoproteinemia Type IIAdaptor Proteins, Signal TransducingHumansInflammasomesInflammationLipoproteins, LDLNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesRNA-Binding ProteinsAdaptor Proteins, Signal TransducingInflammasomesLipoproteins, LDLNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesRNA-Binding ProteinsSORBS2 protein, humanCholesterol effluxNLRP3 inflammasomeOxidized low density lipoproteinROSSORBS2

Identifiers

PMID35590369
PMCPMC9118763
OpenAlexW4280554437

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.