Evidence map›Paper›PMID 41890214›Full record

ArticleFrontiers in cellular neuroscience2026

Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.

Junlong Kang, Wei Li, Xinjie Gao, Xinhua Tian, Wei Feng, Xiang Yao, Feng Wei, Luyue Chen, Hongjin Chen, Junjiang Tong and 2 more

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In one paragraph

Article in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Junlong Kang *Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Wei Li *Department of Pharmacy, The Third Hospital of Xiamen, Xiamen, China.
Xinjie Gao *Department of Neurosurgery, Huashan Hospital of Fudan University, Shanghai, China.
Xinhua TianDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Wei FengDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Xiang YaoDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Feng WeiDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Luyue ChenDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Hongjin ChenDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Junjiang TongDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
E ChenDepartment of Neurosurgery, Zhongshan Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Yuxiang GuDepartment of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The crucial role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in regulating aneurysm formation, inflammation, and neural dysfunction has gradually been recognized. This study aimed to evaluate the effects of MALAT1 modification on pathological changes, inflammation, vascular smooth muscle cell (VSMC) phenotype switching, and the underlying mechanism in intracranial aneurysms (IAs). Methods: MALAT1-overexpressing (oeMALAT1), MALAT1 short hairpin (shMALAT1), and semaphorin 3C (SEMA3C)-overexpressing (oeSEMA3C) lentiviruses were transfected alone or in combination into basilar artery VSMCs originating from IA rats. These lentiviruses were then stereotactically injected into IA rats. Results: Conclusion: Silencing MALAT1 represses pathological progression, inflammation, and VSMC phenotype switching by regulating the SEMA3C-mediated Smad pathway in IA.

Indexed as

intracranial aneurysmMALAT1semaphorin 3Csmadpathwayvascular smooth muscle cells

Identifiers

PMID41890214
PMCPMC13013063

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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.