Related Experiment Video
Updated: Feb 20, 2026

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
STARD4-AS1 promotes coronary artery disease and modulates endothelial dysfunction by targeting miR-204-3p/FLI1
1Department of General Practice, Chinese and Western Medicine Hospital of Panzhihua, Panzhihua, 617000, China.
Background:
Coronary artery disease (CAD) remains the primary cause of mortality and disability-adjusted life years lost worldwide. This study focuses on elucidating the expression, cell functions, and possible regulatory mechanisms of the steroidogenic acute regulator protein-related lipid transfer domain containing 4-antisense RNA 1 (STARD4-AS1) in CAD.
Methods:
GSE113079 dataset was used to identify the studied lncRNA. Serum STARD4-AS1 levels were quantified by RT-qPCR in a cohort of 88 CAD patients and 72 healthy participants. In vitro functional assays were performed in human primary coronary artery endothelial cells (HCAECs) under hypoxia following transfection with STARD4-AS1 siRNA. The cell function assays encompassed monocyte adhesion, lactate dehydrogenase (LDH) release, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and low-density lipoprotein cholesterol (LDL-C). A downstream miRNA for STARD4-AS1 was predicted and validated via dual-luciferase reporter assays. Rescue experiments were conducted for the function assays of STARD4-AS1/miRNA axis.
Results:
GSE113079 dataset revealed a significant elevation of STARD4-AS1 in CAD peripheral blood mononuclear cells. In CAD serum, STARD4-AS1 level was elevated. The STARD4-AS1 upregulation was positively correlated with LDL-C levels and had a diagnostic value for CAD. Under hypoxia, the knockdown of STARD4-AS1 mitigated the LDH release, MDA levels, the intracellular LDL-C content, and monocyte adhesion to HCAECs. MiR-204-3p was identified as a target miRNA for STARD4-AS1, while Friend leukemia virus integration 1 (FLI1) was a target gene for miR-204-3p. MiR-204-3p inhibition can offset the functions of STARD4-AS1 suppression on HCAECs exposed to hypoxic conditions.
Conclusion:
STARD4-AS1 can regulate endothelial cell functions under hypoxic conditions. This study highlights its potential as a novel therapeutic target and a promising circulating biomarker candidate for CAD.
Insights
Steroidogenic acute regulator protein-related lipid transfer domain containing 4-antisense RNA 1 (STARD4-AS1) is elevated in coronary artery disease (CAD) and regulates endothelial cell function. STARD4-AS1 shows potential as a therapeutic target and biomarker for CAD.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Coronary artery disease (CAD) is a leading global cause of mortality.
- Understanding the molecular mechanisms underlying CAD is crucial for developing effective treatments.
- The role of long non-coding RNAs (lncRNAs) like STARD4-AS1 in CAD pathogenesis is under investigation.
Purpose of the Study:
- To investigate the expression, function, and regulatory mechanisms of STARD4-AS1 in CAD.
- To evaluate STARD4-AS1 as a potential diagnostic biomarker for CAD.
- To explore STARD4-AS1 as a therapeutic target for CAD.
Main Methods:
- Analysis of the GSE113079 dataset to identify STARD4-AS1 expression in CAD.
- Quantification of serum STARD4-AS1 levels in CAD patients and healthy controls using RT-qPCR.
- In vitro functional assays in human primary coronary artery endothelial cells (HCAECs) under hypoxia, including siRNA-mediated knockdown of STARD4-AS1, assessment of monocyte adhesion, LDH release, MDA, SOD, and LDL-C levels.
- Prediction and validation of miRNA targets for STARD4-AS1 using dual-luciferase reporter assays.
- Rescue experiments to validate the STARD4-AS1/miRNA axis function.
Main Results:
- STARD4-AS1 was significantly elevated in CAD peripheral blood mononuclear cells and serum.
- Elevated STARD4-AS1 levels correlated positively with LDL-C and demonstrated diagnostic value for CAD.
- Knockdown of STARD4-AS1 in HCAECs under hypoxia reduced LDH release, MDA levels, intracellular LDL-C, and monocyte adhesion.
- MiR-204-3p was identified as a direct target of STARD4-AS1, and FLI1 as a target of miR-204-3p.
- Inhibition of miR-204-3p reversed the protective effects of STARD4-AS1 suppression on hypoxic HCAECs.
Conclusions:
- STARD4-AS1 plays a significant role in regulating endothelial cell function under hypoxic conditions relevant to CAD.
- The STARD4-AS1/miR-204-3p/FLI1 axis is implicated in CAD pathogenesis.
- STARD4-AS1 represents a promising novel therapeutic target and a potential circulating biomarker for CAD.
Related Concept Videos
Coronary Artery Disease II: Pathophysiology
Regulation of Angiogenesis and Blood Supply
Mechanism of Angiogenesis
Coronary Artery Disease I: Introduction
Nitric Oxide Signaling Pathway
TGF - β Signaling Pathway

