Evidence map›Paper›PMID 36070120›Full record

ArticleMolecular neurobiology2022

Inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy.

Chengzhi Han, Xinyi Qian, Xiaorong Ren, Shutian Zhang, Li Hu, Jingyao Li, Yijun Huang, Renhui Huang, Kokwin Ooi, Hong Lin and 1 more

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

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

Chengzhi Han *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Xinyi Qian *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Xiaorong RenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Shutian ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Li HuDepartment of Cardiovascular Diseases, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Jingyao LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Yijun HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Renhui HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Kokwin OoiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Hong LinDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China.
Chunmei XiaDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 130, Dongan Road, Shanghai, 200032, People's Republic of China. cmxia@fudan.edu.cn.ORCID http://orcid.org/0000-0001-9845-9685
Shanghai Medical College of Fudan University · CNFudan University · CNShanghai Jiao Tong University · CN

Funding

Hui-Chun Chin and Tsung-Dao Lee Chinese Undergraduate Research Endowment 2193101011001National Natural Science Foundation of China No. 82171803 and No. 81770423
6 · The paper itself

Abstract

Neuroinflammation in the cardiovascular center plays a critical role in the progression of hypertensive heart disease. And microglial autophagy is involved in the regulation of neuroinflammation. Cyclic GMP-AMP synthase (cGAS), a cytosolic DNA sensor, senses mitochondrial DNA (mtDNA) and regulates autophagy. The detailed mechanisms of central cGAS affects neuroinflammatory response in hypertensive heart disease via regulating autophagy remain unknown. Angiotensin II (Ang II, 1.5 mg·kg

Indexed as

Heart DiseasesHeart InjuriesHypertensionAngiotensin IIAnimalsAutophagyCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialMiceMicrogliaNucleotidyltransferasesParaventricular Hypothalamic NucleusSirolimusAngiotensin IIcGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialNucleotidyltransferasesSirolimusAutophagycGAS-STINGHypertensionMicrogliaNeuroinflammation

Identifiers

PMID36070120
PMCPMC9450841
OpenAlexW4294916441

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.