O-GlcNAcylation Suppresses the Ion Current IClswell by Preventing the Binding of the Protein ICln to α-Integrin

Costa, Roberta; Civello, Davide Antonio; Bernardinelli, Emanuele; Szabó, Z. G.; Morabito, Rossana; Marino, Angela; Sarikas, Antonio; Patsch, Wolfgang; Paulmichl, Markus; Janáky, Tamás; Miseta, Attila; Nagy, Tamás; Dossena, Silvia

doi:10.3389/fcell.2020.607080

Cited by 17 publications

(15 citation statements)

References 96 publications

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“…Moreover, a single episode of severe AKI superimposed on patients with pre-existing CKD can cause further renal deterioration to end-stage kidney disease (ESKD) rapidly at a non-linear pace ( Figure 1 B). The risk factors associated with the AKI-related acceleration of renal progression were identified previously, and include older age, delayed renal function recovery from AKI, severe AKI episodes, the presence of proteinuria, and comorbidities such as DM, hypertension, and heart failure [ 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , ...…”

Section: Avoidance Of Acute Kidney Injury (Aki) In Patients With Ckdmentioning

confidence: 99%

“…In DM, O-GlcNAcylation has a role in insulin resistance and can mediate glucose toxicity, and subsequently, DM complications, including DKD. Recent research has demonstrated that the O-GlcNAcylation of cellular proteins such as ICln impairs cell volume regulation in diverse cell types, a common phenomenon in DM [ 73 ]. A hypertrophic PCT is a typical feature of DKD as increased filtrated glucose promotes the reabsorption of glucose and sodium in PCT.…”

Section: An Etiology-based Treatment Strategy For Ckdmentioning

confidence: 99%

“…Notably, it is found that the renoprotective effect may be extended to non-diabetic patients with kidney diseases [72]. [73]. A hypertrophic PCT is a typical feature of DKD as increased filtrated glucose promotes the reabsorption of glucose and sodium in PCT.…”

Section: Dm-related Ckdmentioning

confidence: 99%

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Chronic Kidney Disease: Strategies to Retard Progression

Yan

Chao

Lin

2021

IJMS

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Chronic kidney disease (CKD), defined as the presence of irreversible structural or functional kidney damages, increases the risk of poor outcomes due to its association with multiple complications, including altered mineral metabolism, anemia, metabolic acidosis, and increased cardiovascular events. The mainstay of treatments for CKD lies in the prevention of the development and progression of CKD as well as its complications. Due to the heterogeneous origins and the uncertainty in the pathogenesis of CKD, efficacious therapies for CKD remain challenging. In this review, we focus on the following four themes: first, a summary of the known factors that contribute to CKD development and progression, with an emphasis on avoiding acute kidney injury (AKI); second, an etiology-based treatment strategy for retarding CKD, including the approaches for the common and under-recognized ones; and third, the recommended approaches for ameliorating CKD complications, and the final section discusses the novel agents for counteracting CKD progression.

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Section: Avoidance Of Acute Kidney Injury (Aki) In Patients With Ckdmentioning

confidence: 99%

Section: An Etiology-based Treatment Strategy For Ckdmentioning

confidence: 99%

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Chronic Kidney Disease: Strategies to Retard Progression

Yan

Chao

Lin

2021

IJMS

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“…O-GlcNAcylation affects many diseases, including diabetes, diabetic nephropathy, and neurodegenerative disease such as Alzheimer disease [11][12][13][14][15]. In recent years, several studies have addressed the role of protein O-GlcNAcylation in various types of cancer, including the impact of O-GlcNAcylation in proliferation, angiogenesis, and metastasis of cancer cells [16,17].…”

Section: Introductionmentioning

confidence: 99%

Role and Function of O-GlcNAcylation in Cancer

Lee

Pyo

Kim

2021

Cancers

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Cancer cells are able to reprogram their glucose metabolism and retain energy via glycolysis even under aerobic conditions. They activate the hexosamine biosynthetic pathway (HBP), and the complex interplay of O-linked N-acetylglucosaminylation (O-GlcNAcylation) via deprivation of nutrients or increase in cellular stress results in the proliferation, progression, and metastasis of cancer cells. Notably, cancer is one of the emerging diseases associated with O-GlcNAcylation. In this review, we summarize studies that delineate the role of O-GlcNAcylation in cancer, including its modulation in metastasis, function with receptor tyrosine kinases, and resistance to chemotherapeutic agents, such as cisplatin. In addition, we discuss the function of O-GlcNAcylation in eliciting immune responses associated with immune surveillance in the tumor microenvironment. O-GlcNAcylation is increasingly accepted as one of the key players involved in the activation and differentiation of T cells and macrophages. Finally, we discuss the prognostic role of O-GlcNAcylation and potential therapeutic agents such as O-linked β-N-acetylglucosamine-transferase inhibitors, which may help overcome the resistance mechanism associated with the reprogramming of glucose metabolism.

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“…It has been the main research focus regarding cancer for decades [46,65]. It is also thought to contribute to the development of diabetic nephropathy by interfering with kidney tubular cells' ion transport, leading to necrotic cell death [66]. Glycosylation is also involved in cardiovascular diseases [67].…”

Section: Glycosylationmentioning

confidence: 99%

Role of Glycosylation in Vascular Calcification

Masbuchin

Rohman

Liu

2021

IJMS

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Glycosylation is an important step in post-translational protein modification. Altered glycosylation results in an abnormality that causes diseases such as malignancy and cardiovascular diseases. Recent emerging evidence highlights the importance of glycosylation in vascular calcification. Two major types of glycosylation, N-glycosylation and O-glycosylation, are involved in vascular calcification. Other glycosylation mechanisms, which polymerize the glycosaminoglycan (GAG) chain onto protein, resulting in proteoglycan (PG), also have an impact on vascular calcification. This paper discusses the role of glycosylation in vascular calcification.

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O-GlcNAcylation Suppresses the Ion Current IClswell by Preventing the Binding of the Protein ICln to α-Integrin

Cited by 17 publications

References 96 publications

Chronic Kidney Disease: Strategies to Retard Progression

Chronic Kidney Disease: Strategies to Retard Progression

Role and Function of O-GlcNAcylation in Cancer

Role of Glycosylation in Vascular Calcification

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