Video Experimental Relacionado

Updated: Feb 20, 2026

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

STARD4-AS1 promueve la enfermedad de las arterias coronarias y modula la disfunción endotelial al dirigirse a

Yuan Li¹, Li Liu¹

¹Department of General Practice, Chinese and Western Medicine Hospital of Panzhihua, Panzhihua, 617000, China.

Microvascular research

|February 18, 2026

Abstracto

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.

Palabras clave:

Biomarcador Enfermedad de las arterias coronarias Estrés oxidativo STARD4-AS1 miR-204-3p

Más Videos Relacionados

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Delivery of Modified mRNA in a Myocardial Infarction Mouse Model

Delivery of Modified mRNA in a Myocardial Infarction Mouse Model

Published on: June 11, 2020

Videos de Conceptos Relacionados

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

Coronary Artery Disease I: Introduction

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...

Nitric Oxide Signaling Pathway

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...

TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...