Evidence map›Paper›PMID 35783850›Full record

ReviewFrontiers in cardiovascular medicine2022

Endoplasmic Reticulum Stress and Pathogenesis of Vascular Calcification.

Zhenqi Rao, Yidan Zheng, Li Xu, Zihao Wang, Ying Zhou, Ming Chen, Nianguo Dong, Zhejun Cai, Fei Li

Open access · goldAbstract readReview
In one paragraph

Review 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Emerging role of IRE1α in vascular diseases.Journal of cell communication and signaling · 2024
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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 3 institutions in 1 country.

Zhenqi RaoDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yidan ZhengBasic Medical School, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Li XuDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zihao WangDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ying ZhouDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ming ChenDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Nianguo DongDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhejun CaiDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Fei LiDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Union Hospital · CNHuazhong University of Science and Technology · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.

Indexed as

atherosclerosischronic kidney diseasediabetesendoplasmic reticulum stressunfolded protein responsevascular calcification

Identifiers

PMID35783850
PMCPMC9243238
OpenAlexW4282965695

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.