Evidence map›Paper›PMID 33828087›Full record

ArticleCell death & disease2021

Loss of FoxO3a prevents aortic aneurysm formation through maintenance of VSMC homeostasis.

Weiling Lu, Yu Zhou, Shan Zeng, Lintao Zhong, Shiju Zhou, Haoyu Song, Rongming Ding, Gaojun Zhong, Qingrui Li, Yuhua Hu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 43 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

19 authors at 6 institutions in 1 country.

Weiling Lu *Department of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Yu Zhou *Division of Vascular Surgery, National-Local Joint Engineering Laboratory of Vascular Disease Treatment, Engineering and Technology Center for Diagnosis and Treatment of Vascular Diseases, Guangdong Engineering Laboratory of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Shan Zeng *Department of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Lintao Zhong *Department of Cardiology, Zhuhai People's Hospital (Zhuhai Hospital Affiliated with Jinan University), 519000, Zhuhai, China.
Shiju ZhouDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Haoyu SongWards of Cadres, Zhuhai People's Hospital (Zhuhai Hospital Affiliated with Jinan University), 519000, Zhuhai, China.
Rongming DingDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Gaojun ZhongDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Qingrui LiDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Yuhua HuDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Zhongyu WenDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Qin LiaoDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Yalan WangDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Lianglliang LyuDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Yiming ZhongDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Gonghua HuDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China.
Yulin LiaoDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, 510515, Guangzhou, China. liao18@msn.com.ORCID 0000-0001-5961-390X
Dongming XieDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China. xiedongminggy@163.com.ORCID 0000-0002-9604-7123
Jiahe XieDepartment of Cardiology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, First Affiliated Hospital of Gannan Medical University, Gannan Medical University, University Town, Ganzhou Development District, 341000, Ganzhou, China. xiejiahezg@126.com.ORCID 0000-0001-8410-4330
First Affiliated Hospital of Gannan Medical University · CNGannan Medical University · CNJinan University · CNGanzhou People's Hospital · CNNanfang Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle cell (VSMC) phenotypic switching plays a critical role in the formation of abdominal aortic aneurysms (AAAs). FoxO3a is a key suppressor of VSMC homeostasis. We found that in human and animal AAA tissues, FoxO3a was upregulated, SM22α and α-smooth muscle actin (α-SMA) proteins were downregulated and synthetic phenotypic markers were upregulated, indicating that VSMC phenotypic switching occurred in these diseased tissues. In addition, in cultured VSMCs, significant enhancement of FoxO3a expression was found during angiotensin II (Ang II)-induced VSMC phenotypic switching. In vivo, FoxO3a overexpression in C57BL/6J mice treated with Ang II increased the formation of AAAs, whereas FoxO3a knockdown exerted an inhibitory effect on AAA formation in ApoE

Indexed as

AnimalsAortic AneurysmForkhead Box Protein O3HomeostasisHumansMaleMiceMuscle, Smooth, VascularTransfectionForkhead Box Protein O3FOXO3 protein, human

Identifiers

PMID33828087
PMCPMC8027644
OpenAlexW3150260443

What Socratic 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 Socratic graph.