Evidence map›Paper›PMID 39969669›Full record

ArticleGeneral thoracic and cardiovascular surgery2025

WTAP-mediated m6A modification on BASP1 mRNA contributes to ferroptosis in AAA.

Zexiang Tian, Wei Li, Jian Wang, Shuzhen Li

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Article in General thoracic and cardiovascular surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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4citing papers in PubMed
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4 citing papers in PubMed.

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5 · Who and what money

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4 authors.

Zexiang TianDepartment of Cardiothoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No.1, Tongdao North Street, Huimin District, Hohhot, 010050, China.
Wei LiDepartment of Cardiothoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No.1, Tongdao North Street, Huimin District, Hohhot, 010050, China.
Jian WangDepartment of Cardiothoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No.1, Tongdao North Street, Huimin District, Hohhot, 010050, China.
Shuzhen LiDepartment of Cardiothoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No.1, Tongdao North Street, Huimin District, Hohhot, 010050, China. 15389712647@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbdominal aortic aneurysm (AAA) is a common aneurysm that is often associated with atherosclerosis and can lead to artery rupture and death. Brain abundant membrane attached signal protein 1 (BASP1) is related to a variety of pathophysiological processes, but its role in AAA has not been reported.

methodsReal-time quantitative polymerase chain reaction (qRT-PCR) and western blot were used to detect the expressions of BASP1 and Wilms' tumor 1-associated protein (WTAP). Angiotensin-II (Ang-II) was employed for inducing AAA models in vitro to explore the effects and mechanism of BASP1 in AAA. Cell viability, apoptosis, oxidative stress level, and Fe

resultsA highly expressed level of BASP1 was observed in aortic tissues of AAA patients and Ang-II could induce AAA models by treating vascular smooth muscle cells (VSMCs). In cellular function, BASP1 knockdown impaired AAA and ferroptosis resulted from Ang-II. Mechanically, WTAP mediated the N6-methyladenosine (m6A) modification and mRNA stability of BASP1. Meanwhile, WTAP was highly expressed in AAA tissues of patients and the effects of WTAP silence in AAA and ferroptosis were diminished by up-regulated BASP1.

conclusionWTAP promotes cell viability and inhibits apoptosis and ferroptosis resulted from Ang-II in VSMCs by mediating the m6A level of BASP1.

Indexed as

Adaptor Proteins, Signal TransducingAdenosineAortic Aneurysm, AbdominalFerroptosisMembrane ProteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleNerve Tissue ProteinsRNA, MessengerAngiotensin IIAnimalsCell Cycle ProteinsFemaleHumansMaleOxidative StressAdaptor Proteins, Signal TransducingAdenosineAngiotensin IIBASP1 protein, humanCell Cycle ProteinsMembrane ProteinsNerve Tissue ProteinsN-methyladenosineRepressor ProteinsRNA, MessengerRNA Splicing FactorsWTAP protein, humanAbdominal aortic aneurysmBrain abundant membrane attached signal protein 1FerroptosisN 6-methyladenosineWilms’ tumor 1-associated protein

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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.