Non-coding RNA-mediated modulation of ferroptosis in cardiovascular diseases

Liu, Ying; Ding, Wei; Jx, Wang; Ao, Xiang; Xue, Junqiang

doi:10.1016/j.biopha.2023.114993

Cited by 41 publications

(58 citation statements)

References 144 publications

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“…Supporting this, GFAT inhibitors have been observed to decrease overall O‐GlcNAcylation in SHR and significantly reduce BP 205 . The administration of deoxycorticosterone acetate salt elevated ET‐1 levels and induced increased BP in hypertensive rats by upregulating vascular GFAT expression and promoting O‐GlcNAcylation 206,207 …”

Section: Role Of O‐glcnacylation In Diseasesmentioning

confidence: 90%

O‐GlcNAcylation: cellular physiology and therapeutic target for human diseases

Ye,

Ding,

Xiao

et al. 2023

MedComm

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O‐linked‐β‐N‐acetylglucosamine (O‐GlcNAcylation) is a distinctive posttranslational protein modification involving the coordinated action of O‐GlcNAc transferase and O‐GlcNAcase, primarily targeting serine or threonine residues in various proteins. This modification impacts protein functionality, influencing stability, protein–protein interactions, and localization. Its interaction with other modifications such as phosphorylation and ubiquitination is becoming increasingly evident. Dysregulation of O‐GlcNAcylation is associated with numerous human diseases, including diabetes, nervous system degeneration, and cancers. This review extensively explores the regulatory mechanisms of O‐GlcNAcylation, its effects on cellular physiology, and its role in the pathogenesis of diseases. It examines the implications of aberrant O‐GlcNAcylation in diabetes and tumorigenesis, highlighting novel insights into its potential role in cardiovascular diseases. The review also discusses the interplay of O‐GlcNAcylation with other protein modifications and its impact on cell growth and metabolism. By synthesizing current research, this review elucidates the multifaceted roles of O‐GlcNAcylation, providing a comprehensive reference for future studies. It underscores the potential of targeting the O‐GlcNAcylation cycle in developing novel therapeutic strategies for various pathologies.

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Section: Role Of O‐glcnacylation In Diseasesmentioning

confidence: 90%

O‐GlcNAcylation: cellular physiology and therapeutic target for human diseases

Ye,

Ding,

Xiao

et al. 2023

MedComm

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“…■ FUNCTIONAL ROLES OF CIRCNFIXS IN DIFFERENT PHYSIOLOGICAL PROCESSES circNFIX (2) and circNFIX (3,4,5,6,7,8) have been identified to participate in diverse physiological processes, such as myogenesis, heart disease progression, 25,67,70 cancer pathogenesis, 27,47,71 etc. (Figure 3; Table 2).…”

Section: ■ Characteristics Of Circnfixmentioning

confidence: 99%

“…94 Glioma is difficult to cure and easily recur. (3,4,5,6,7,8) was overexpressed in glioma. 27 Bioinformatic analysis, RIP assays and dualluciferase reporter assays showed that circNFIX (3,4,5,6,7,8) could bind to miR-34a-5p and downregulate its expression.…”

Section: ■ Characteristics Of Circnfixmentioning

confidence: 99%

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The Role of Circular RNA Variants Generated from the NFIX Gene in Different Diseases

Zhang,

Li,

Gao

et al. 2024

Mol. Pharmaceutics

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Circular RNAs (circRNAs) have been identified as important regulators in different developmental processes and disease pathogenesis. The loop structure of circRNAs makes them very stable in different conditions and microenvironments. circRNAs can affect microRNA (miRNA) and RNA binding protein (RBP) activity, encode functional proteins and regulate gene transcription. Recently, two circNFIX variants derived from the same gene, the Nuclear Factor I X (NFIX) gene, were determined as participants in the pathological processes of various diseases such as heart diseases and cancers. Both circNFIX variants are exonic circular RNAs and mainly function by sponging miRNAs. In this review, we summarize the current knowledge on circRNAs, elucidate the origins and properties of two circNFIX variants, explore the roles of two circNFIX variants in different diseases, and present clinical perspectives.

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“…Some studies have shown that copper-induced mitochondrial apoptosis is characterized by increased expression of bax, bak, caspase 3, caspase 8, and caspase 9 [34,35] the activation of which is a signature of cell apoptosis. [36] Other studies have shown that copper-induced cell death is mediated by caspase 1, a signature of another type of programmed cell death called pyroptosis. [37,38] Furthermore, copperinduced cell death is also reported to be caspase independent [39] but points more toward a process marked by endoplasmic reticulum stress and massive vacuolization in the absence of apoptotic features.…”

Section: Copper-induced Cell Death and Cuproptosismentioning

confidence: 99%

Copper and Diabetes: Current Research and Prospect

Chang,

2023

Molecular Nutrition Food Res

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Copper is an essential trace metal for normal cellular functions; a lack of copper is reported to impair the function of important copper‐binding enzymes, while excess copper could lead to cell death. Numerous studies have shown an association between dietary copper consumption or plasma copper levels and the incidence of diabetes/diabetes complications. And experimental studies have revealed multiple signaling pathways that are triggered by copper shortages or copper overload in diabetic conditions. Moreover, studies show that treated with copper chelators improve vascular function, maintain copper homeostasis, inhibit cuproptosis, and reduce cell toxicity, thereby alleviating diabetic neuropathy, retinopathy, nephropathy, and cardiomyopathy. However, the mechanisms reported in these studies are inconsistent or even contradictory. This review summarizes the precise and tight regulation of copper homeostasis processes, and discusses the latest progress in the association of diabetes and dietary copper/plasma copper. Further, the study pays close attention to the therapeutic potential of copper chelators and copper in diabetes and its complications, and hopes to provide new insight for the treatment of diabetes.

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Non-coding RNA-mediated modulation of ferroptosis in cardiovascular diseases

Cited by 41 publications

References 144 publications

O‐GlcNAcylation: cellular physiology and therapeutic target for human diseases

O‐GlcNAcylation: cellular physiology and therapeutic target for human diseases

The Role of Circular RNA Variants Generated from the NFIX Gene in Different Diseases

Copper and Diabetes: Current Research and Prospect

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