Evidence map›Paper›PMID 35990936›Full record

ArticleFrontiers in cardiovascular medicine2022

YB1 dephosphorylation attenuates atherosclerosis by promoting CCL2 mRNA decay.

Yaqin Tang, Zhiwei Li, Hongqin Yang, Yang Yang, Chi Geng, Bin Liu, Tiantian Zhang, Siyang Liu, Yunfei Xue, Hongkai Zhang and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Targeted drug delivery systems for atherosclerosis.Journal of nanobiotechnology · 2025
    Review
  3. Article
  4. 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

12 authors at 3 institutions in 2 countries.

Yaqin TangState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Zhiwei LiState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Hongqin YangState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Yang YangState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Chi GengState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Bin LiuJilin Zhongtai Biotechnology Co., Ltd, Jilin, China.
Tiantian ZhangState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Siyang LiuState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Yunfei XueState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Hongkai ZhangThe Pathology Department, Beijing Hospital of Traditional Chinese Medicine, The Capital Medical University, Beijing, China.
Jing WangState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Hongmei ZhaoState Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNKai Biotech (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is a key pathological process in atherosclerosis. RNA binding proteins (RBPs) have been reported to play an important role in atherosclerotic plaque formation, and they could regulate the expression of inflammatory factors by phosphorylation modification. Y-box binding protein 1 (YB1) is an RBP that has participated in many inflammatory diseases. Here, we found an increased expression of phosphorylated YB1 (pYB1) in atherosclerotic plaques and demonstrated that YB1 dephosphorylation reduced lipid accumulation and lesion area in the aorta

Indexed as

atherosclerosisinflammationmRNA decayphosphorylationRNA binding protein

Identifiers

PMID35990936
PMCPMC9386362
OpenAlexW4289745424

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.