High glucose induced endothelial to mesenchymal transition in human umbilical vein endothelial cell

Yu, Chun-Hong; Suriguga, Su; Gong, Meng; Liu, Wenjuan; Cui, Ning-Xuan; Wang, Ying; Du, Xin; Zhang, Yi

doi:10.1016/j.yexmp.2017.03.007

Cited by 54 publications

(55 citation statements)

References 33 publications

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“…As mentioned before, TGF-β is a key regulator of ECM, thus its excessive signaling has long been implicated in the pathogenesis of vascular fibrosis and other fibrosis-related diseases. Moreover, it acts as a mediator of vascular fibrosis induced by several agents involved in vascular diseases (e.g., mechanical stress, angiotensin II, high glucose, advanced glycation products) [ 22 , 72 , 82 , 83 ]. The heat shock protein 70 (HSP70), whose primary function is to repair denatured proteins through folding/unfolding steps and thus achieve correct functional configuration, is another example of an agent believed to stimulate TGFβ1-induced ECM accumulation and to contribute to the inflammation and fibrosis present in fibrosis-related diseases [ 84 ].…”

Section: The Role Of Tgf-β1 Signaling Pathways In Vessel Wall Pathmentioning

confidence: 99%

TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology

Serralheiro

Soares

Almeida

et al. 2017

IJMS

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Chronic venous insufficiency and varicose veins occur commonly in affluent countries and are a socioeconomic burden. However, there remains a relative lack of knowledge about venous pathophysiology. Various theories have been suggested, yet the molecular sequence of events is poorly understood. Transforming growth factor-beta one (TGF-β1) is a highly complex polypeptide with multifunctional properties that has an active role during embryonic development, in adult organ physiology and in the pathophysiology of major diseases, including cancer and various autoimmune, fibrotic and cardiovascular diseases. Therefore, an emphasis on understanding its signaling pathways (and possible disruptions) will be an essential requirement for a better comprehension and management of specific diseases. This review aims at shedding more light on venous pathophysiology by describing the TGF-β1 structure, function, activation and signaling, and providing an overview of how this growth factor and disturbances in its signaling pathway may contribute to specific pathological processes concerning the vessel wall which, in turn, may have a role in chronic venous insufficiency.

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Section: The Role Of Tgf-β1 Signaling Pathways In Vessel Wall Pathmentioning

confidence: 99%

TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology

Serralheiro

Soares

Almeida

et al. 2017

IJMS

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“…P65, encoded by RELA gene, is activated by fatty acids and hyperglycaemia in heart . Although increasing evidence suggests that high glucose concentration is associated with EndMT in ECs, the mechanism underlying the regulation of EndMT in T1DM is still unclear …”

Section: Introductionmentioning

confidence: 99%

“…9 Although increasing evidence suggests that high glucose concentration is associated with EndMT in ECs, the mechanism underlying the regulation of EndMT in T1DM is still unclear. 28 miRNAs constitute a class of short, 20-23-nucleotide-long, non-coding RNA. 29 Recently, the parts of miRNAs in cardiac fibrosis have been confirmed, thereby revealing a new mechanism underlying the regulation of cardiac diseases.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‐21 alleviated cardiac perivascular fibrosis via repressing EndMT in T1DM

Yao

Shi

et al. 2019

J Cellular Molecular Medi

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In type 1 and type 2 diabetes mellitus, increased cardiac fibrosis, stiffness and associated diastolic dysfunction may be the earliest pathological phenomena in diabetic cardiomyopathy. Endothelial‐mesenchymal transition (EndMT) in endothelia cells (ECs) is a critical cellular phenomenon that increases cardiac fibroblasts (CFs) and cardiac fibrosis in diabetic hearts. The purpose of this paper is to explore the molecular mechanism of miR‐21 regulating EndMT and cardiac perivascular fibrosis in diabetic cardiomyopathy. In vivo, hyperglycaemia up‐regulated the mRNA level of miR‐21, aggravated cardiac dysfunction and collagen deposition. The condition was recovered by inhibition of miR‐21 following with improving cardiac function and decreasing collagen deposition. miR‐21 inhibition decreased cardiac perivascular fibrosis by suppressing EndMT and up‐regulating SMAD7 whereas activating p‐SMAD2 and p‐SMAD3. In vitro, high glucose (HG) up‐regulated miR‐21 and induced EndMT in ECs, which was decreased by inhibition of miR‐21. A highly conserved binding site of NF‐κB located in miR‐21 5′‐UTR was identified. In ECs, SMAD7 is directly regulated by miR‐21. In conclusion, the pathway of NF‐κB/miR‐21/SMAD7 regulated the process of EndMT in T1DM, in diabetic cardiomyopathy, which may be regarded as a potential clinical therapeutic target for cardiac perivascular fibrosis.

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“…Studies have demonstrated that genetic defect associated with metabolic syndrome such as dyslipidemia and hyperglycemia induces the accumulation of oxidized low-density lipoprotein (ox-LDL) and glucose respectively. Ectopic accumulation of ox-LDL and glucose further enhance inflammation, EndMT and monocyte/macrophage adhesion via NF-кB pathway leading to AS progression [ 19 , 20 ], indicating that AS can be triggered by multiple mechanisms. Targeting these mechanisms may provide a technique for the prevention of AS.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms and genetic regulation in atherosclerosis

Jackson

Regine

Subrata

et al. 2018

IJC Heart & Vasculature

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Atherosclerosis (AS) manifested by lipid accumulation, extracellular matrix protein deposition, and calcification in the intima and media of the large to medium size arteries promoting arterial stiffness and reduction of elasticity. It has been accepted that AS leads to increased morbidity and mortality worldwide. Recent studies indicated that genetic abnormalities play an important role in the development of AS. Specific genetic mutation and histone modification have been found to induce AS formation. Furthermore, specific RNAs such as microRNAs and circular RNAs have been identified to play a crucial role in the progression of AS. Nevertheless, the mechanisms by which genetic mutation, DNA and histone modification, microRNAs and circular RNA induce AS still remain elusive. This review describes specific mechanisms and pathways through which genetic mutation, DNA and histone modification, microRNAs and circular RNA instigate AS. This review further provides a therapeutic strategic direction for the treatment of AS targeting genetic mechanisms.

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High glucose induced endothelial to mesenchymal transition in human umbilical vein endothelial cell

Cited by 54 publications

References 33 publications

TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology

TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology

Inhibition of miR‐21 alleviated cardiac perivascular fibrosis via repressing EndMT in T1DM

Molecular mechanisms and genetic regulation in atherosclerosis

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