CircHIPK3 Regulates Vascular Smooth Muscle Cell Calcification Via the miR-106a-5p/MFN2 Axis

Zhang, Wen-Bo; Qi, You-Fei; Zhanxiang, Xiao; Chen, Hao; Sahua, Liu; Li, Zhenzhen; Zeng, Zhaofan; Wu, Huimeng

doi:10.1007/s12265-022-10247-8

Cited by 11 publications

(13 citation statements)

References 39 publications

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“…In another article on AS, the expression of miR-106a is upregulated in cells treated by ox-LDL and it participates in the activity of cells [ 26 ]. The level of miR-126 is elevated in the tissues and blood samples of patients with AS [ 27 ]. Additionally, LKB1 was tested as a directly targeted gene of miR-106a.…”

Section: Discussionmentioning

confidence: 99%

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Rui¹,

Rong³

et al. 2023

BMC Cardiovasc Disord

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Background Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. Methods The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. Results The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. Conclusion Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.

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Section: Discussionmentioning

confidence: 99%

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Rui¹,

Rong³

et al. 2023

BMC Cardiovasc Disord

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“…On the other hand, overexpression of circHIPK3 resulted in sponging of miR-190b and increased activity of the ATG7 pathway, which correlated with reduced lipid accumulation and promoted autophagy (Figure 4). 1) and ( 4) harmful effects of cellular proliferation, migration, and apoptosis [61,82], and ( 2) and ( 3) protective effects of inhibited osteogenic differentiation, mineralization, and calcium deposition, reduced lipid accumulation, and increased rates of autophagy [37,143]. Both (1) harmful and (2) protective effects were seen from sponging of miR-106a-5p [82].…”

Section: Circhipk3mentioning

confidence: 99%

“…Opposing effects on angiogenesis were also demonstrated via sponging of miR-637 by (4) circHIPK3 and [61] (5) circ_0002194 [122], the latter of which suggests equivocal effects on the pathogenesis of atherosclerosis due to the observed impaired angiogenesis but enhanced oxidative stress. 1) and ( 4) harmful effects of cellular proliferation, migration, and apoptosis [61,82], and ( 2) and (3) protective effects of inhibited osteogenic differentiation, mineralization, and calcium deposition, reduced lipid accumulation, and increased rates of autophagy [37,143]. Both (1) harmful and (2) protective effects were seen from sponging of miR-106a-5p [82].…”

Section: Circhipk3mentioning

confidence: 99%

Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?

Triska

Mathew

Zhao

et al. 2023

JCM

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Much attention has been paid lately to harnessing the diagnostic and therapeutic potential of non-coding circular ribonucleic acids (circRNAs) and micro-RNAs (miRNAs) for the prevention and treatment of cardiovascular diseases. The genetic environment that contributes to atherosclerosis pathophysiology is immensely complex. Any potential therapeutic application of circRNAs must be assessed for risks, benefits, and off-target effects in both the short and long term. A search of the online PubMed database for publications related to circRNA and atherosclerosis from 2016 to 2022 was conducted. These studies were reviewed for their design, including methods for developing atherosclerosis and the effects of the corresponding atherosclerotic environment on circRNA expression. Investigated mechanisms were recorded, including associated miRNA, genes, and ultimate effects on cell mechanics, and inflammatory markers. The most investigated circRNAs were then further analyzed for redundant, disparate, and/or contradictory findings. Many disparate, opposing, and contradictory effects were observed across experiments. These include levels of the expression of a particular circRNA in atherosclerotic environments, attempted ascertainment of the in toto effects of circRNA or miRNA silencing on atherosclerosis progression, and off-target, cell-specific, and disease-specific effects. The high potential for detrimental and unpredictable off-target effects downstream of circRNA manipulation will likely render the practice of therapeutic targeting of circRNA or miRNA molecules not only complicated but perilous.

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“…The reports on miRNA involvement in the regulatory network of cardiovascular disease have shown the upregulation of miR-106a in cardiac hypertrophy, and mitofusin 2 (Mfn2) was identified as the potential target gene for this miRNA. Mfn2, a key member of the mitofusin protein family, is located in the outer membrane of mitochondria and acts to maintain this organelle’s structure [ 145 , 146 ]. Mfn2 is known as a cell proliferation suppressor gene, probably by inhibiting the MAPK/ERK pathway.…”

Section: Mir-106a: Dysregulation In Non-cancer Diseasesmentioning

confidence: 99%

Overview of miR-106a Regulatory Roles: from Cancer to Aging

Daneshpour

Ghadimi-Daresajini

2023

Bioengineering

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MicroRNAs (miRNAs) comprise a class of non-coding RNA with extensive regulatory functions within cells. MiR-106a is recognized for its super-regulatory roles in vital processes. Hence, the analysis of its expression in association with diseases has attracted considerable attention for molecular diagnosis and drug development. Numerous studies have investigated miR-106 target genes and shown that this miRNA regulates the expression of some critical cell cycle and apoptosis factors, suggesting miR-106a as an ideal diagnostic and prognostic biomarker with therapeutic potential. Furthermore, the reported correlation between miR-106a expression level and cancer drug resistance has demonstrated the complexity of its functions within different tissues. In this study, we have conducted a comprehensive review on the expression levels of miR-106a in various cancers and other diseases, emphasizing its target genes. The promising findings surrounding miR-106a suggest its potential as a valuable biomolecule. However, further validation assessments and overcoming existing limitations are crucial steps before its clinical implementation can be realized.

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CircHIPK3 Regulates Vascular Smooth Muscle Cell Calcification Via the miR-106a-5p/MFN2 Axis

Cited by 11 publications

References 39 publications

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?

Overview of miR-106a Regulatory Roles: from Cancer to Aging

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