Vitamin D-VDR (vitamin D receptor) regulates defective autophagy in renal tubular epithelial cell in streptozotocin-induced diabetic mice via the AMPK pathway

Li, Aimei; Yi, Bin; Han, Hailong; Yang, Shikun; Hu, Zhaoxin; Li, Zheng; Wang, Jianwen; Liao, Qin; Zhang, Hao

doi:10.1080/15548627.2021.1962681

Cited by 75 publications

(72 citation statements)

References 47 publications

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“…PCV2 induces autophagy via the CaMKKβ-AMPK pathway in pig kidney PK-15 cells by increasing cytosolic Ca 2+ [113]. Activation of vitamin D receptors can restore defective autophagy through the Ca 2+ -CAMKKβ-AMPK pathway in renal tubular epithelial cells in streptozotocin-induced diabetic mice [114]. Ca 2+ signaling is involved in AMPK-mediated autophagy, and plays a role in coordinating cellular survival and kidney function.…”

Section: Targeted Ca 2+ Signaling For Therapy Of Kidney Diseasesmentioning

confidence: 96%

“…Saikosaponin-d (SSd), a SERCA inhibitor, suppresses excess ER Ca 2+ reuptake and cell proliferation in ADPKD cells by inducing autophagy through the CaMKKβ-AMPK-mTOR signaling pathway, which indicates that SSd might be a potential treatment for ADPKD and that SERCA might be a novel target for ADPKD therapy [117]. It has been reported that AMPK activation restored the defective autophagy in high glucose-induced HK-2 cells [114]. Activators of CaSR such as cinacalcet have renoprotective effects in high glucose-treated human glomerular endothelial cells, murine podocytes and diabetic mice.…”

Section: Targeted Ca 2+ Signaling For Therapy Of Kidney Diseasesmentioning

confidence: 99%

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Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

Niu

Guo

Kong

et al. 2021

Cells

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The kidney is an important organ for the maintenance of Ca2+ homeostasis in the body. However, disruption of Ca2+ homeostasis will cause a series of kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), renal ischemia/reperfusion (I/R) injury, autosomal dominant polycystic kidney disease (ADPKD), podocytopathy, and diabetic nephropathy. During the progression of kidney disease, Ca2+ signaling plays key roles in various cell activities such as necrosis, apoptosis, eryptosis and autophagy. Importantly, there are complex Ca2+ flux networks between the endoplasmic reticulum (ER), mitochondria and lysosomes which regulate intracellular Ca2+ signaling in renal cells and contribute to kidney disease. In addition, Ca2+ signaling also links the crosstalk between various cell deaths and autophagy under the stress of heavy metals or high glucose. In this regard, we present a review of Ca2+ signaling in cell death and crosstalk with autophagy and its potential as a therapeutic target for the development of new and efficient drugs against kidney diseases.

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Section: Targeted Ca 2+ Signaling For Therapy Of Kidney Diseasesmentioning

confidence: 96%

Section: Targeted Ca 2+ Signaling For Therapy Of Kidney Diseasesmentioning

confidence: 99%

Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

Niu

Guo

Kong

et al. 2021

Cells

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“…Several animal studies have shown that 25(OH)D 3 concentrations are significantly lower in DN compared to healthy controls, suggesting that vitamin D plays a significant role in the development of DN [ 15 , 16 ]. In mice and rats with DN, a significantly lower expression of the VDR gene has been observed [ 18 ].…”

Section: Animal Studiesmentioning

confidence: 99%

“…Studies in rats and mice have investigated whether supplementation with vitamin D might have a renoprotective role in the process of developing DN [ 15 , 16 , 18 , 19 , 20 , 21 , 22 ]. In the study of Hamzawy et al [ 20 ], 30 diabetic rats were divided into three groups: group 1 (the control group), group 2 (the DN group), and group 3 (the vitamin D-treated DN group).…”

Section: Animal Studiesmentioning

confidence: 99%

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The Role of Vitamin D in Diabetic Nephropathy: A Translational Approach

Delrue

Speeckaert

Delanghe

et al. 2022

IJMS

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According to several animal and human studies, vitamin D appears to play a significant role in the development of diabetic nephropathy. However, the possible renoprotective effect of vitamin D and its influence on the reversal of already existing renal damage remains doubtful. At this moment, there are a few hypotheses concerning the underlying molecular and genetic mechanisms including the link between vitamin D and inflammation, oxidative stress, and extracellular matrix accumulation. The present review aims to investigate the potential role of vitamin D in the development of diabetic kidney disease from a translational approach.

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VDR Activation Attenuates Renal Tubular Epithelial Cell Ferroptosis by Regulating Nrf2/HO‐1 Signaling Pathway in Diabetic Nephropathy

Wang,

Yu,

Liu

et al. 2023

Advanced Science

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Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. Ferroptosis, a new form of cell death, plays a crucial role in the pathogenesis of DN. Renal tubular injury triggered by ferroptosis might be essential in this process. Numerous studies demonstrate that the vitamin D receptor (VDR) exerts beneficial effects by suppressing ferroptosis. However, the underlying mechanism has not been fully elucidated. Thus, they verified the nephroprotective effect of VDR activation and explored the mechanism by which VDR activation suppressed ferroptosis in db/db mice and high glucose‐cultured proximal tubular epithelial cells (PTECs). Paricalcitol (PAR) is a VDR agonist that can mitigate kidney injury and prevent renal dysfunction. PAR treatment could inhibit ferroptosis of PTECs through decreasing iron content, increasing glutathione (GSH) levels, reducing malondialdehyde (MDA) generation, decreasing the expression of positive ferroptosis mediator transferrin receptor 1 (TFR‐1), and enhancing the expression of negative ferroptosis mediators including ferritin heavy chain (FTH‐1), glutathione peroxidase 4 (GPX4), and cystine/glutamate antiporter solute carrier family 7 member 11 (SLC7A11). Mechanistically, VDR activation upregulated the NFE2‐related factor 2/heme oxygenase‐1 (Nrf2/HO‐1) signaling pathway to suppress ferroptosis in PTECs. These findings suggested that VDR activation inhibited ferroptosis of PTECs in DN via modulating the Nrf2/HO‐1 signaling pathway.

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Vitamin D-VDR (vitamin D receptor) regulates defective autophagy in renal tubular epithelial cell in streptozotocin-induced diabetic mice via the AMPK pathway

Abstract: Zhang (2021): Vitamin D-VDR (vitamin D receptor) regulates defective autophagy in renal tubular epithelial cell in streptozotocin-induced diabetic mice via the AMPK pathway, Autophagy,

Cited by 75 publications

References 47 publications

Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

The Role of Vitamin D in Diabetic Nephropathy: A Translational Approach

VDR Activation Attenuates Renal Tubular Epithelial Cell Ferroptosis by Regulating Nrf2/HO‐1 Signaling Pathway in Diabetic Nephropathy

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