Upregulation of nuclear factor‐κB activity mediates CYP24 expression and reactive oxygen species production in indoxyl sulfate‐induced chronic kidney disease

Wang, Lihua; Gao, Zhiying; Wang, Lili; Gao, Yongning

doi:10.1111/nep.12673

Cited by 17 publications

(19 citation statements)

References 41 publications

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“…IL-1β, TNF-α) in a rat model of diabetic nephropathy 46 . Consistently, others have also reported that chronic kidney disease induced by indoxyl sulfate in rats resulted in marked oxidative stress and inflammation through the up-regulation of VD catabolising enzyme 47 . Similar results have also been observed in testicular tissues following treatment of diabetic rats with VD 45 , 48 .…”

Section: Discussionsupporting

confidence: 68%

“…Similar results have also been observed in testicular tissues following treatment of diabetic rats with VD 45 , 48 . Hence, we speculate that the observed pathological alterations in cellular VD system following Pb poisoning could be an additional mechanism by which the heavy metal promotes oxidative stress, inflammation and subsequently damages kidney and testis tissues 47 . In support with our suggestion above, VD 3 in our study resulted in significant alleviations in renal and testicular tissue injuries observed in animals exposed to Pb-only.…”

Section: Discussionmentioning

confidence: 92%

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Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats

BaSalamah

Abdelghany

El‐Boshy

et al. 2018

Sci Rep

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This study measured the effects of vitamin D (VD) supplementation on the underlying molecular pathways involved in renal and testicular damage induced by lead (Pb) toxicity. Thirty two adult male Wistar rats were divided equally into four groups that were treated individually or simultaneously, except the negative control, for four weeks with lead acetate in drinking water (1,000 mg/L) and/or intramuscular VD (1,000 IU/kg; 3 days/week). Pb toxicity markedly reduced serum VD and Ca2+, induced substantial renal and testicular injuries with concomitant significant alterations in the expression of VD metabolising enzymes, its receptor and binding protein, and the calcium sensing receptor. Pb also significantly promoted lipid peroxidation and pro-inflammatory cytokines (IL-4 and TNF-α) in the organs of interest concomitantly with declines in several anti-oxidative markers (glutathione, glutathione peroxidase and catalase) and the anti-inflammatory cytokine, IL-10. The co-administration of VD with Pb markedly mitigated renal and testicular injuries compared with positive controls. This was associated with restoration of the expression of VD related molecules, promotion of anti-oxidative and anti-inflammatory markers, but tissue Pb concentrations were unaffected. In conclusion, this report is the first to reveal potential protective effects for VD against Pb-induced renal and testicular injuries via anti-inflammatory and anti-oxidative mechanisms.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 92%

Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats

BaSalamah

Abdelghany

El‐Boshy

et al. 2018

Sci Rep

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“…Vitamin D deficiency is common in CKD and diabetes mellitus for several reasons: (1) renal deterioration and proteinuria [100][101][102], (2) reduced 1-alpha hydroxylase activity within the kidney [103,104], (3) increased catabolism of 25(OH)D into inactive metabolite 24,25(OH)2D [103,105], and (4) pharmacological concentrations of vitamin D [106]. Current active vitamin D supplements have microgram concentrations [107].…”

Section: Possible Therapeutic Roles Of Vitamin D In Mscs and Vascularmentioning

confidence: 99%

The Role of Vitamin D in Modulating Mesenchymal Stem Cells and Endothelial Progenitor Cells for Vascular Calcification

Hou

Zheng

et al. 2020

IJMS

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Vascular calcification, which involves the deposition of calcifying particles within the arterial wall, is mediated by atherosclerosis, vascular smooth muscle cell osteoblastic changes, adventitial mesenchymal stem cell osteoblastic differentiation, and insufficiency of the calcification inhibitors. Recent observations implied a role for mesenchymal stem cells and endothelial progenitor cells in vascular calcification. Mesenchymal stem cells reside in the bone marrow and the adventitial layer of arteries. Endothelial progenitor cells that originate from the bone marrow are an important mechanism for repairing injured endothelial cells. Mesenchymal stem cells may differentiate osteogenically by inflammation or by specific stimuli, which can activate calcification. However, the bioactive substances secreted from mesenchymal stem cells have been shown to mitigate vascular calcification by suppressing inflammation, bone morphogenetic protein 2, and the Wingless-INT signal. Vitamin D deficiency may contribute to vascular calcification. Vitamin D supplement has been used to modulate the osteoblastic differentiation of mesenchymal stem cells and to lessen vascular injury by stimulating adhesion and migration of endothelial progenitor cells. This narrative review clarifies the role of mesenchymal stem cells and the possible role of vitamin D in the mechanisms of vascular calcification.

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“…CKD progression in addition to tubulointerstitial damage reduced the activity of 1- α -hydroxylase and 25-hydroxylase. In addition, in uremic rats, indoxyl sulfate upregulated nuclear factor- κ B expression in renal tubular cells and subsequently activated 24-hydroxylase [ 21 , 22 ]. Increased 24-hydroxylase and decreased 1- α -hydroxylase activities cause a prominent reduction of endogenous 25(OH)D and 1,25(OH)2D products, thus increasing their decay.…”

Section: Vitamin D Deficiency In Patients With Ckd: Mechanism ( mentioning

confidence: 99%

“…Fetuin-A is synthesized in the liver as a negative acute-phase protein. Low fetuin-A reflects malnutrition in patients undergoing HD, and low serum fetuin-A is associated with more severe vascular calcification and subsequent cardiovascular mortality [ 22 ]. MGP, synthesized by VSMCs [ 59 ], is observed at the interface between normal tissues and the mineralized lesions of calcified arteries in patients with CKD or diabetes mellitus.…”

Section: The Mechanisms Of Cardiovascular Calcification In Ckdmentioning

confidence: 99%

Role of Vitamin D in Uremic Vascular Calcification

Hou

Liu

Zheng

et al. 2017

BioMed Research International

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The risk of cardiovascular death is 10 times higher in patients with CKD (chronic kidney disease) than in those without CKD. Vascular calcification, common in patients with CKD, is a predictor of cardiovascular mortality. Vitamin D deficiency, another complication of CKD, is associated with vascular calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial injury, and the therapeutic dose of active form vitamin D aggravate vitamin D deficiency and reduce its pleiotropic effect on the cardiovascular system. Vitamin D supplement for CKD patients provides a protective role in vascular calcification on the endothelium by (1) renin-angiotensin-aldosterone system inactivation, (2) alleviating insulin resistance, (3) reduction of cholesterol and inhibition of foam cell and cholesterol efflux in macrophages, and (4) modulating vascular regeneration. For the arterial calcification, vitamin D supplement provides adjunctive role in regressing proteinuria, reverse renal osteodystrophy, and restoring calcification inhibitors. Recently, adventitial progenitor cell has been linked to be involved in the vascular calcification. Vitamin D may provide a role in modulating adventitial progenitor cells. In summary, vitamin D supplement may provide an ancillary role for ameliorating uremic vascular calcification.

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Upregulation of nuclear factor‐κB activity mediates CYP24 expression and reactive oxygen species production in indoxyl sulfate‐induced chronic kidney disease

Cited by 17 publications

References 41 publications

Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats

Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats

The Role of Vitamin D in Modulating Mesenchymal Stem Cells and Endothelial Progenitor Cells for Vascular Calcification

Role of Vitamin D in Uremic Vascular Calcification

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