Evidence map›Paper›PMID 29147891›Full record

ArticleImmunologic research2018

Long-term presence of angiotensin II type 1 receptor autoantibody reduces aldosterone production by triggering Ca

Jinghui Lei, Suli Zhang, Pengli Wang, Yang Liao, Jingwei Bian, Xiaochen Yin, Ye Wu, Lina Bai, Feng Wang, Xiaoli Yang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

11 authors at 3 institutions in 1 country.

Jinghui LeiDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Suli ZhangDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Pengli WangDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Yang LiaoDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Jingwei BianDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Xiaochen YinDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Ye WuDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Lina BaiDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China.
Feng WangDepartment of Pathophysiology, Key Laboratory of Cell Physiology of Ministry of Education,The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
Xiaoli YangDepartment of Reproductive Center, Taiyuan Central Hospital, Taiyuan, Shanxi, 030009, China. yxl00124@126.com.
Huirong LiuDepartment of Physiology & Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men Street, Beijing, 100069, China. liuhr2000@126.com.
Capital Medical University · CNShanxi Medical University · CNTaiyuan Central Hospital · CN

Funding

National Natural Science Foundation of China 81471478National Natural Science Foundation of China 91539205Natural Science Foundation of Shanxi Province, China 201601D011093
6 · The paper itself

Abstract

Preeclamptic women are reported to have inadequate plasma volume expansion coupled with a suppressed secretion of aldosterone; however, the specific mechanism of preeclampsia remains unclear. We demonstrated that the presence of long-term angiotensin II type 1 receptor autoantibody (AT1-AA) reduces aldosterone production by triggering a Ca

Indexed as

Adrenal Cortex NeoplasmsAldosteroneAutoantibodiesAutoantigensCalciumCalcium ChannelsCalcium SignalingCell DeathCell Line, TumorFemaleHumansPre-EclampsiaPregnancyProtein Kinase CReceptor, Angiotensin, Type 1AldosteroneAutoantibodiesAutoantigensCalciumCalcium ChannelsProtein Kinase CReceptor, Angiotensin, Type 1AldosteroneAngiotensin receptorAutoantibodyPreeclampsia

Identifiers

PMID29147891
OpenAlexW2769370295

What OpenQuestion holds

Textmetadata
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.