Circ_0068087 Silencing Ameliorates Oxidized Low-Density Lipoprotein-Induced Dysfunction in Vascular Endothelial Cells Depending on miR-186-5p-Mediated Regulation of Roundabout Guidance Receptor 1

Li, Shuanghong; Huang, Tao; Qin, Linling; Yin, Lu

doi:10.3389/fcvm.2021.650374

Cited by 16 publications

(9 citation statements)

References 39 publications

(45 reference statements)

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“…Serving as the sponge of miR-876-3p, the Circ_0093887 has also been reported to help protect HAECs against the oxLDL-induced inflammatory and apoptotic damages ( 39 ). Furthermore, for the circ_0068087, with similar targeted ROBO1 expression in circ-USP36, it not only aggravates hyperglycemia-induced dysfunction and inflammation of ECs with a sponge of miR-197 in diabetes but also alleviated oxLDL-induced dysfunction in HUVECs partly accompanied by reducing and upregulating miR-186-5p ( 42 ).…”

Section: Oxldl and Endothelial Cell Dysfunctionmentioning

confidence: 99%

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

Jiang

Zhou

Nabavi³

et al. 2022

Front. Cardiovasc. Med.

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Atherosclerosis is an immuno-metabolic disease involving chronic inflammation, oxidative stress, epigenetics, and metabolic dysfunction. There is compelling evidence suggesting numerous modifications including the change of the size, density, and biochemical properties in the low-density lipoprotein (LDL) within the vascular wall. These modifications of LDL, in addition to LDL transcytosis and retention, contribute to the initiation, development and clinical consequences of atherosclerosis. Among different atherogenic modifications of LDL, oxidation represents a primary modification. A series of pathophysiological changes caused by oxidized LDL (oxLDL) enhance the formation of foam cells and atherosclerotic plaques. OxLDL also promotes the development of fatty streaks and atherogenesis through induction of endothelial dysfunction, formation of foam cells, monocyte chemotaxis, proliferation and migration of SMCs, and platelet activation, which culminate in plaque instability and ultimately rupture. This article provides a concise review of the formation of oxLDL, enzymes mediating LDL oxidation, and the receptors and pro-atherogenic signaling pathways of oxLDL in vascular cells. The review also explores how oxLDL functions in different stages of endothelial dysfunction and atherosclerosis. Future targeted pathways and therapies aiming at reducing LDL oxidation and/or lowering oxLDL levels and oxLDL-mediated pro-inflammatory responses are also discussed.

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Section: Oxldl and Endothelial Cell Dysfunctionmentioning

confidence: 99%

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

Jiang

Zhou

Nabavi³

et al. 2022

Front. Cardiovasc. Med.

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“…In addition, Zhang et al declared that SNHG7 sponged miR-186-5p to modulate endothelial cells’ phenotype [ 20 ]. More importantly, Li et al suggested that miR-186-5p exerted a protective role by downregulating ROBO1 in ox-LDL-exposed human umbilical vein endothelial cells [ 39 ]. Nevertheless, the function of miR-186-5p in CAD is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Circ_ROBO2/miR-186-5p/TRIM14 axis regulates oxidized low-density lipoprotein-induced cardiac microvascular endothelial cell injury

Zhou

et al. 2022

Regenerative Therapy

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“…The circ_0068087 expression level was increased in blood sample from patients with T2D. Circ_0068087 knockdown could ameliorate ox-LDL-induced HUVEC dysfunction by miR-186-5p and roundabout guidance receptor 1 (ROBO1) ( Li et al, 2021a ). Moreover, circ_0068087 knockdown could also suppress cell dysfunction under HG conditions.…”

Section: Vascular Damage Due To Hyperglycemia and Dyslipidemiamentioning

confidence: 99%

The mechanisms of glycolipid metabolism disorder on vascular injury in type 2 diabetes

Chen

Shi²,

Wang

et al. 2022

Front. Physiol.

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Patients with diabetes have severe vascular complications, such as diabetic nephropathy, diabetic retinopathy, cardiovascular disease, and neuropathy. Devastating vascular complications lead to increased mortality, blindness, kidney failure, and decreased overall quality of life in people with type 2 diabetes (T2D). Glycolipid metabolism disorder plays a vital role in the vascular complications of T2D. However, the specific mechanism of action remains to be elucidated. In T2D patients, vascular damage begins to develop before insulin resistance and clinical diagnosis. Endothelial dysregulation is a significant cause of vascular complications and the early event of vascular injury. Hyperglycemia and hyperlipidemia can trigger inflammation and oxidative stress, which impair endothelial function. Furthermore, during the pathogenesis of T2D, epigenetic modifications are aberrant and activate various biological processes, resulting in endothelial dysregulation. In the present review, we provide an overview and discussion of the roles of hyperglycemia- and hyperlipidemia-induced endothelial dysfunction, inflammatory response, oxidative stress, and epigenetic modification in the pathogenesis of T2D. Understanding the connections of glucotoxicity and lipotoxicity with vascular injury may reveal a novel potential therapeutic target for diabetic vascular complications.

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Circ_0068087 Silencing Ameliorates Oxidized Low-Density Lipoprotein-Induced Dysfunction in Vascular Endothelial Cells Depending on miR-186-5p-Mediated Regulation of Roundabout Guidance Receptor 1

Cited by 16 publications

References 39 publications

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

Circ_ROBO2/miR-186-5p/TRIM14 axis regulates oxidized low-density lipoprotein-induced cardiac microvascular endothelial cell injury

The mechanisms of glycolipid metabolism disorder on vascular injury in type 2 diabetes

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