Evidence map›Paper›PMID 29296021›Full record

ArticleNature communications2018

Homocysteine directly interacts and activates the angiotensin II type I receptor to aggravate vascular injury.

Tuoyi Li, Bing Yu, Zhixin Liu, Jingyuan Li, Mingliang Ma, Yingbao Wang, Mingjiang Zhu, Huiyong Yin, Xiaofeng Wang, Yi Fu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
20.5field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 254 citations in OpenAlex.

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  8. Copy number loss Of APP cause thoracic aortic dissection.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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6 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 3 countries.

Tuoyi LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Bing YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Zhixin LiuDepartment of Biochemistry and Molecular Biology, School of Medicine, Shandong University; Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, 250012, China.
Jingyuan LiCAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, 19 B, Yuquan Road, Beijing, 100049, China.
Mingliang MaDepartment of Biochemistry and Molecular Biology, School of Medicine, Shandong University; Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, 250012, China.
Yingbao WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Mingjiang ZhuKey Laboratory of Food Safety Research, Institute for Nutritional Sciences (INS), Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, 200031, China.
Huiyong YinKey Laboratory of Food Safety Research, Institute for Nutritional Sciences (INS), Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, 200031, China.ORCID http://orcid.org/0000-0001-7049-1560
Xiaofeng WangCAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, 19 B, Yuquan Road, Beijing, 100049, China.
Yi FuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Fang YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Xian WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Xiaohong FangKey Laboratory of Molecular Nanostructure and Nanotechnology, CAS Research/Education Center for Excellence in Molecular Sciences, Institute of Chemistry, Chinese Academy of Sciences, Beijing, 100190, China.
Jinpeng SunDepartment of Biochemistry and Molecular Biology, School of Medicine, Shandong University; Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, 250012, China. sunjinpeng@sdu.edu.cn.
Wei KongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China. kongw@bjmu.edu.cn.
Ministry of Education of the People's Republic of China · CNChinese Academy of Sciences · CNInstitute of High Energy Physics · CNMinistry of Education · ROShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is a risk factor for various cardiovascular diseases. However, the mechanism underlying HHcy-aggravated vascular injury remains unclear. Here we show that the aggravation of abdominal aortic aneurysm by HHcy is abolished in mice with genetic deletion of the angiotensin II type 1 (AT1) receptor and in mice treated with an AT1 blocker. We find that homocysteine directly activates AT1 receptor signalling. Homocysteine displaces angiotensin II and limits its binding to AT1 receptor. Bioluminescence resonance energy transfer analysis reveals distinct conformational changes of AT1 receptor upon binding to angiotensin II and homocysteine. Molecular dynamics and site-directed mutagenesis experiments suggest that homocysteine regulates the conformation of the AT1 receptor both orthosterically and allosterically by forming a salt bridge and a disulfide bond with its Arg

Indexed as

Allosteric RegulationAngiotensin IAngiotensin IIAnimalsAortic Aneurysm, AbdominalHEK293 CellsHomocysteineHumansMaleMice, Inbred C57BLMolecular Dynamics SimulationMutagenesis, Site-DirectedProtein ConformationReceptor, Angiotensin, Type 1Vascular System InjuriesAngiotensin IAngiotensin IIHomocysteineReceptor, Angiotensin, Type 1

Identifiers

PMID29296021
PMCPMC5750214
OpenAlexW2780027234

What OpenQuestion holds

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Registered trials

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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.