Evidence map›Paper›PMID 37301198›Full record

ArticleCell reports. Medicine2023

Targeting cytokine-like protein FAM3D lowers blood pressure in hypertension.

Yicong Shen, Zhigang Dong, Fangfang Fan, Kaiyin Li, Shirong Zhu, Rongbo Dai, Jiaqi Huang, Nan Xie, Li He, Ze Gong and 11 more

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

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 15 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

21 authors at 4 institutions in 1 country.

Yicong ShenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Zhigang DongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Fangfang FanState Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Department of Cardiology, Institute of Cardiovascular Disease, Peking University First Hospital, Beijing 100034, China.
Kaiyin LiState Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Department of Cardiology, Institute of Cardiovascular Disease, Peking University First Hospital, Beijing 100034, China.
Shirong ZhuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Rongbo DaiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Jiaqi HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Nan XieDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Shenzhen Key Laboratory of Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, Guangdong 518057, China.
Li HeDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, China.
Ze GongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Xueyuan YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Jiaai TanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Limei LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Fang YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Yida TangState Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing 100191, China.
Zhen YouDepartment of Biliary Surgery, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Jianzhong XiDepartment of Biomedicine, College of Engineering, Peking University, Beijing 100871, China.
Ying WangDepartment of Immunology, School of Basic Medical Sciences, and Key Laboratory of Medical Immunology of Ministry of Health, Peking University, Beijing 100191, China.
Wei KongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China. Electronic address: kongw@bjmu.edu.cn.
Yan ZhangState Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Department of Cardiology, Institute of Cardiovascular Disease, Peking University First Hospital, Beijing 100034, China. Electronic address: drzhy1108@163.com.
Yi FuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China. Electronic address: yi.fu@bjmu.edu.cn.
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNSichuan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current antihypertensive options still incompletely control blood pressure, suggesting the existence of uncovered pathogenic mechanisms. Here, whether cytokine-like protein family with sequence similarity 3, member D (FAM3D) is involved in hypertension etiology is evaluated. A case-control study exhibits that FAM3D is elevated in patients with hypertension, with a positive association with odds of hypertension. FAM3D deficiency significantly ameliorates angiotensin II (AngII)-induced hypertension in mice. Mechanistically, FAM3D directly causes endothelial nitric oxide synthase (eNOS) uncoupling and impairs endothelium-dependent vasorelaxation, whereas 2,4-diamino-6-hydroxypyrimidine to induce eNOS uncoupling abolishes the protective effect of FAM3D deficiency against AngII-induced hypertension. Furthermore, antagonism of formyl peptide receptor 1 (FPR1) and FPR2 or the suppression of oxidative stress blunts FAM3D-induced eNOS uncoupling. Translationally, targeting endothelial FAM3D by adeno-associated virus or intraperitoneal injection of FAM3D-neutralizing antibodies markedly ameliorates AngII- or deoxycorticosterone acetate (DOCA)-salt-induced hypertension. Conclusively, FAM3D causes eNOS uncoupling through FPR1- and FPR2-mediated oxidative stress, thereby exacerbating the development of hypertension. FAM3D may be a potential therapeutic target for hypertension.

Indexed as

CytokinesHypertensionAnimalsBlood PressureCase-Control StudiesHumansMiceVasodilationCytokinesFAM3D protein, humanFAM3D protein, mouseantihypertensive treatmentendothelial dysfunctionFAM3Dhypertension

Identifiers

PMID37301198
PMCPMC10313939
OpenAlexW4380203853

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.