lncMALAT1在冠状动脉疾病中的作用及信号通路：一项体内和体外研究的系统评价方案
The roles and signalling pathways of lncMALAT1 in coronary artery disease: A protocol for systematic review of in vivo and in vitro studies.
作者信息
Zheng Jia, Mat Ludin Arimi Fitri, Rajab Nor Fadilah, Shaolong Li, Jufri Nurul Farhana
机构信息
Department of Cardiovascular Surgery, Yan'an Hospital affiliated to Kunming Medical University, Kunming, China.
Center for Toxicology and Health Risk Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
出版信息
PLoS One. 2025 May 5;20(5):e0322550. doi: 10.1371/journal.pone.0322550. eCollection 2025.
BACKGROUND
Coronary artery disease (CAD) is a major cardiovascular disease that affects global population health. Several studies have indicated the association between high expression level of a non-coding RNA, lncMALAT1 and an increased risk of CAD. In this study, we conducted a protocol of systematic review aims to evaluate the role and mechanism of lncMALAT1 that may contributed to CAD based on animal and in vitro studies. The roles of lncMALAT1 will be elucidated focusing on activating upstream signalling Klotho/FGF23 or regulate the downstream Wnt/β-catenin or extracellular signal-regulated kinase/mitogen-activated protein kinase(ERK/MAPK) and any other pathways with the vascular changes in term of proliferation, migration, lumen formation and apoptosis.
METHODS
A systematic review protocol with a reproducible strategy according to the Preferred Reporting Items for Systematic Review and Meta-analysis Protocols (PRISMA-P) guidelines and Population, Intervention, Comparison Outcome and Study (PICOS) framework were proposed to evaluate the existing literature on the roles and mechanisms of the lncMALAT1. A PRISMA-compliant electrical systematic research was performed in the databases including PubMed, Web of Science and Scopus for English publication from their inceptions until January 2024. Data for collection will include primary CAD animal models and any cardiomyocyte cell line with primary hypoxia model. The article title, authors, type of models, signaling pathways and biological changes (proliferation, migration, lumen formation and apoptosis) will be recorded.
CONCLUSION
This will provide a new approach in understanding molecular interactions on CAD for new perspective and target treatment for CAD patients in future, especially that intolerance of invasive coronary therapy.
REGISTRATION
Registered in PROSPERO on 10 April, 2024. (CRD42024504245) (https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024504245).
背景
冠状动脉疾病（CAD）是一种影响全球人口健康的主要心血管疾病。多项研究表明，非编码RNA lncMALAT1的高表达水平与CAD风险增加之间存在关联。在本研究中，我们开展了一项系统评价方案，旨在基于动物和体外研究评估lncMALAT1可能导致CAD的作用和机制。将重点阐明lncMALAT1的作用，即激活上游信号通路Klotho/FGF23或调节下游Wnt/β-连环蛋白或细胞外信号调节激酶/丝裂原活化蛋白激酶（ERK/MAPK）以及任何其他与血管在增殖、迁移、管腔形成和凋亡方面变化相关的通路。
方法
根据系统评价与Meta分析方案的首选报告项目（PRISMA-P）指南和人群、干预措施、对照、结局和研究（PICOS）框架，提出了一项具有可重复策略的系统评价方案，以评估关于lncMALAT1作用和机制的现有文献。在包括PubMed、科学网和Scopus在内的数据库中进行了符合PRISMA标准的电子系统研究，以获取从创刊至2024年1月的英文出版物。收集的数据将包括原发性CAD动物模型和任何具有原发性缺氧模型的心肌细胞系。将记录文章标题、作者、模型类型、信号通路和生物学变化（增殖、迁移、管腔形成和凋亡）。
结论
这将为从新的视角理解CAD中的分子相互作用提供一种新方法，并为未来CAD患者，尤其是对侵入性冠状动脉治疗不耐受的患者提供靶向治疗。
注册情况
于2024年4月10日在PROSPERO注册。（CRD号：CRD42024504245）（https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024504245）
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