CircRNA CDR1as promotes cardiomyocyte apoptosis through activating hippo signaling pathway in diabetic cardiomyopathy

Shao, Yingchun; Li, Mengmeng; Qi, Yu; Gong, Manyu; Wang, Yanying; Yang, Xuewen; Liu, Liheng; Liu, Dongping; Tan, Zhongyue; Zhang, Yuanyuan; Qu, Yunmeng; Li, Haodong; Wang, Yaqi; Jiao, Lei; Zhang, Ying

doi:10.1016/j.ejphar.2022.174915

Cited by 42 publications

(21 citation statements)

References 34 publications

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“…In reference to the previous literatures, we speculated that the intrinsic mechanism of this phenomenon may be attributed to the ubiquitination modification of circRNAs on the stability of protein translated from downstream target genes. Such findings have been reported frequently, for example, circ‐CDR1as activated the hippo signaling pathway by significantly inhibiting MST1 ubiquitination level, thereby promoting cardiomyocyte apoptosis in diabetic cardiomyopathy (Shao et al, 2022). Circ‐Foxo3 promoted MDM2‐induced p53 ubiquitination and degradation, resulting in an overall decrease of p53 (W. W. Du et al, 2017).…”

Section: Discussionsupporting

confidence: 63%

Circular RNA SESN2 aggravates gestational trophoblast cell damage induced by high glucose by binding to IGF2BP2

Huang

Guo

2023

Molecular Reproduction Devel

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Gestational diabetes mellitus (GDM) is a common disease in pregnant women that threatens maternal and fetal health. Circular RNAs (circRNAs) have been considered potential diagnostic markers for GDM and affect trophoblast cell phenotypes. This study aimed to explore the effect of circSESN2 on high glucose (HG)-treated trophoblast cells. Peripheral blood and placental tissues were taken from patients with GDM, in which circSESN2 and IGF2BP2 levels were detected by quantitative reverse transcription polymerase chain reaction and/or western blot. HTR-8/SVneo cells were treated with 25 mM glucose and transduced with circSESN2 or IGF2BP2 knockdown vectors. HTR-8/SVneo cell viability was evaluated by MTT assay, cell migration by scratch test, and cell invasion by transwell assay, IL-1β, IL-6, TNF-α, malondialdehyde, and superoxide dismutase levels by ELISA or kits, and reactive oxygen species levels by DCFH-DA probes. The binding between circSESN2 and IGF2BP2 was verified by RNA pulldown and RIP assays. CircSESN2 and IGF2BP2 were overexpressed in GDM patients. Suppressing circSESN2 or IGF2BP2 increased HTR-8/SVneo cell invasion and migration, decreased cell apoptosis, and reduced pro-inflammatory cytokine release and oxidative stress injury. CircSESN2 bound IGF2BP2 and IGF2BP2 overexpression accelerated HG-induced HTR-8/SVneo cell damage despite circSESN2 knockdown. Collectively, circSESN2 exacerbated HG-induced trophoblast cell damage by binding IGF2BP2 and upregulating its protein expression.

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Section: Discussionsupporting

confidence: 63%

Circular RNA SESN2 aggravates gestational trophoblast cell damage induced by high glucose by binding to IGF2BP2

Huang

Guo

2023

Molecular Reproduction Devel

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“…This induced large tumor suppressor kinases 1/2 (LATS1/ 2), which ultimately inactivated YAP1 via phosphorylation. 153 This finding contrasts the results from ischemic regenerating 54 and reperfused 145 myocardium where ALKBH5 and FTO, respectively, were found to upregulate YAP1 via other mechanisms. Similarly, increasing m 6 A by METTL14 overexpression appeared therapeutic through suppression of nucleotide-binding oligomerization domain-like receptor (NLR) family pyrin domain containing 3 (NLRP3)-mediated cardiomyocyte pyroptosis, which was firmly linked with a m 6 A-dependent and YTHDF2-mediated degradation of lncRNA terminal differentiation-induced non-coding RNA (TINCR).…”

Section: Cardiac Hypertrophy and Failurementioning

confidence: 68%

“…While METTL14 appeared downregulated in a mouse model of diabetic cardiomyopathy, 152 ALKBH5 was upregulated and, contrary to its function in ischemia, 134 promoted cardiomyocyte apoptosis ultimately via YAP1 inactivation. 153 Mechanistically, in high-glucose-treated cardiomyocytes, ALKBH5 was unveiled to demethylate forkhead box O3 ( Foxo3 ) mRNA m 6 A, upregulate the protein, and activate the transcription of circular RNA cerebellar degeneration-related protein 1 antisense RNA (circ-CDR1as), which enabled blockage of ubiquitination of mammalian sterile 20-like kinase 1 (MST1). This induced large tumor suppressor kinases 1/2 (LATS1/2), which ultimately inactivated YAP1 via phosphorylation.…”

Section: N 6 -Methyladenosine and A-to-i Modificat...mentioning

confidence: 99%

Emerging roles of the RNA modifications N6-methyladenosine and adenosine-to-inosine in cardiovascular diseases

Sikorski¹,

Vento²,

Kankuri³

2022

Molecular Therapy - Nucleic Acids

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“…NcRNAs play an important role in the process of DM-induced CVD. As previously described, aberrantly expressed ncRNAs promote cardiomyocyte death or endothelial injury (142,148,149). NcRNAs bring new perspectives for the prevention and treatment of diabetic CVD.…”

Section: Discussionmentioning

confidence: 86%

“…The lncRNA ZFAS1 can act as a molecular sponge for miR-150-5p, and, when ZFAS1 is inhibited it, can reduce iron death and combat diabetic cardiomyopathy by activating CCND2 ( 147 ). CircCDR1as promotes cardiomyocyte apoptosis in diabetic cardiomyopathy by activating the hippo signaling pathway; in contrast, circHIPK3 is downregulated in diabetic cardiomyopathy and protects cardiomyocytes from high-glucose-induced apoptosis when overexpressed ( 148 , 149 ). Reducing the expression of lncRNA TINCR and MIAT inhibit cell scorching and alleviate diabetic cardiomyopathy, the former by enhancing the mRNA stability of NLRP3 and the latter by acting as a molecular sponge for miR-214-3p ( 150 , 151 ).…”

Section: Ncrnas In Diabetic Cardiovascular Diseasementioning

confidence: 99%

Non-coding RNAs in diabetes mellitus and diabetic cardiovascular disease

Wang

Jiang

et al. 2022

Front. Endocrinol.

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More than 10% of the world’s population already suffers from varying degrees of diabetes mellitus (DM), but there is still no cure for the disease. Cardiovascular disease (CVD) is one of the most common and dangerous of the many health complications that can be brought on by DM, and has become the leading cause of death in people with diabetes. While research on DM and associated CVD is advancing, the specific mechanisms of their development are still unclear. Given the threat of DM and CVD to humans, the search for new predictive markers and therapeutic ideas is imminent. Non-coding RNAs (ncRNAs) have been a popular subject of research in recent years. Although they do not encode proteins, they play an important role in living organisms, and they can cause disease when their expression is abnormal. Numerous studies have observed aberrant ncRNAs in patients with DM complications, suggesting that they may play an important role in the development of DM and CVD and could potentially act as biomarkers for diagnosis. There is additional evidence that treatment with existing drugs for DM, such as metformin, alters ncRNA expression levels, suggesting that regulation of ncRNA expression may be a key mechanism in future DM treatment. In this review, we assess the role of ncRNAs in the development of DM and CVD, as well as the evidence for ncRNAs as potential therapeutic targets, and make use of bioinformatics to analyze differential ncRNAs with potential functions in DM.

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CircRNA CDR1as promotes cardiomyocyte apoptosis through activating hippo signaling pathway in diabetic cardiomyopathy

Cited by 42 publications

References 34 publications

Circular RNA SESN2 aggravates gestational trophoblast cell damage induced by high glucose by binding to IGF2BP2

Circular RNA SESN2 aggravates gestational trophoblast cell damage induced by high glucose by binding to IGF2BP2

Emerging roles of the RNA modifications N6-methyladenosine and adenosine-to-inosine in cardiovascular diseases

Non-coding RNAs in diabetes mellitus and diabetic cardiovascular disease

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