The roles and signalling pathways of lncMALAT1 in coronary artery disease: A protocol for systematic review of in vivo and in vitro studies

TL;DR

This paper outlines a systematic review protocol to explore how a non-coding RNA called lncMALAT1 contributes to coronary artery disease through various signaling pathways.

Contribution

The study introduces a systematic review protocol to investigate lncMALAT1's role in coronary artery disease using in vivo and in vitro models.

Findings

lncMALAT1 is associated with increased CAD risk and may influence vascular changes through Klotho/FGF23, Wnt/β-catenin, and ERK/MAPK pathways.

The systematic review will focus on proliferation, migration, lumen formation, and apoptosis in CAD models.

The protocol follows PRISMA-P and PICOS frameworks to ensure reproducibility and comprehensive data collection.

Abstract

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.

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.

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.

Registered in PROSPERO on 10 April, 2024. (CRD42024504245) (https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024504245).

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