The complex biology of the arterial wall: much more than endothelial dysfunction and atherosclerosis

Crea, Filippo

doi:10.1093/eurheartj/ehaa926

Cited by 3 publications

(2 citation statements)

References 16 publications

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“…As a chronic inflammatory disease, atherosclerosis (AS) has been considered to induce severe clinical complications, such as cerebral infarction, cardiovascular disease, and peripheral vascular diseases [1,2]. Currently, it is reported that aberrant endothelial cell injury is one of the leading causes of artery atheromatous plaque, which eventually leads to the progression of atherosclerosis [3,4]. Of note, numerous researchers have discovered that oxidized low-density lipoprotein (ox-LDL) is able to trigger the apoptosis of endothelial cells and is considered as an important risk factor for AS [5,6].…”

Section: Introductionmentioning

confidence: 99%

Oxidized low-density lipoprotein contributes to injury of endothelial cells via the circ_0090231/miR-9-5p/TXNIP axis

Lei¹,

Yang²

2022

cejoi

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Atherosclerosis (AS) has been reported to induce severe clinical complications. Circular RNA (circRNA) circ_0090231 was found to be aberrantly overexpressed in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cells. This study was designed to explore the role and mechanism of circ_0090231 in ox-LDL-triggered endothelial cell injury in AS. Circ_0090231,, and thioredoxin interacting protein (TXNIP) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, angiogenesis, and apoptosis were detected by 3-( 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), tube formation, and flow cytometry assay. Bcl-2, Bax, and TXNIP protein levels were gauged by western blot assay. Malondialdehyde (MDA), lactate dehydrogenase (LDH), and superoxide dismutase (SOD) activity were determined by special kits. Tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin 6 (IL-6) levels were analyzed using enzyme-linked immunosorbent assay (ELISA) kits. The binding relationship between miR-9-5p and circ_0090231 or TXNIP was predicted by starBase, and then verified by a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0090231 and TXNIP were increased, and miR-9-5p was decreased in ox-LDL-treated HUVECs. Moreover, circ_0090231 knockdown mitigated ox-LDL-induced HUVEC injury by boosting angiogenesis, oxidative stress, and inflammation, and hindering apoptosis. The mechanical analysis revealed that circ_0090231 acted as a sponge of miR-9-5p to regulate TXNIP expression. Circ_0090231 could attenuate ox-LDL-mediated HUVEC damage by the miR-9-5p/TXNIP axis, providing a promising therapeutic strategy for AS treatment.

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Section: Introductionmentioning

confidence: 99%

Oxidized low-density lipoprotein contributes to injury of endothelial cells via the circ_0090231/miR-9-5p/TXNIP axis

Lei¹,

Yang²

2022

cejoi

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show abstract

“…As a complex inflammatory disorder, atherosclerosis (AS) was reported to be accompanied by severe clinical complications, like coronary heart disease, cerebral infarction, and peripheral vascular diseases 1,2 . Accumulating evidence proved that endothelial cell injury contributed to form the artery atheromatous plaque, eventually leading to the pathogenesis and progression of AS 3–5 . Of note, oxidized low‐density lipoprotein (ox‐LDL) could accelerate the levels of adhesion molecules and chemokines, thereby causing that ox‐LDL was regarded as a crucial contributor and risk factor of AS development 6 .…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV protects against oxidized low‐density lipoprotein‐induced injury in human umbilical vein endothelial cells via the histone deacetylase 9 (HDAC9)/NF‐κB axis

Chen

et al. 2022

Environmental Toxicology

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Background: Atherosclerosis is a main cause of multiple cardiovascular diseases, and cell damage of human umbilical vein endothelial cells (HUVECs) was reported to participate in the development of atherosclerosis. In this study, we aimed to study the action of Astragaloside IV (ASV) on AS development using in vitro AS cell model.Methods: MTT assay, EdU staining assay, and flow cytometry were utilized for detection of cell proliferation and apoptosis, respectively. The protein expression of histone deacetylase 9 (HDAC9), Bax, Bcl-2, p-P65, P65, p-IκBα, and IκBα was gaged using western blot. The angiogenesis was evaluated by tube formation assay. The inflammatory response was evaluated by ELISA kits. SOD activity and MDA level were detected using the matched commercial kits. RT-qPCR was used for HDAC9 mRNA expression measurement.Results: Oxidized low-density lipoprotein (ox-LDL) significantly repressed cell proliferation, angiogenesis, and enhanced apoptosis, inflammation, and oxidative stress in HUVECs. ASV addition could alleviate ox-LDL-caused cell damage in HUVECs. Moreover, HDAC9 was overexpressed in AS patients and AS cell model. Functionally, HDAC9 knockdown also exhibited the protective role in ox-LDL-treated HUVECs. In addition, ASV treatment protected against ox-LDL-induced damage in HUVECs via targeting HDAC9. ASV could inactivate the NF-κB pathway via regulating HDAC9 in AS cell model. Conclusion:ASV exerted the protective effects on ox-LDL-induced damage in HUVECs through the HDAC9/NF-κB axis.

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Trimethylamine-N-oxide (TMAO) promotes balloon injury-induced neointimal hyperplasia via upregulating Beclin1 and impairing autophagic flux

Hong¹,

Que²,

Zhong³

et al. 2022

Biomedicine & Pharmacotherapy

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The complex biology of the arterial wall: much more than endothelial dysfunction and atherosclerosis

Cited by 3 publications

References 16 publications

Oxidized low-density lipoprotein contributes to injury of endothelial cells via the circ_0090231/miR-9-5p/TXNIP axis

Oxidized low-density lipoprotein contributes to injury of endothelial cells via the circ_0090231/miR-9-5p/TXNIP axis

Astragaloside IV protects against oxidized low‐density lipoprotein‐induced injury in human umbilical vein endothelial cells via the histone deacetylase 9 (HDAC9)/NF‐κB axis

Trimethylamine-N-oxide (TMAO) promotes balloon injury-induced neointimal hyperplasia via upregulating Beclin1 and impairing autophagic flux

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