Diverse Role of TGF-β in Kidney Disease

Gu, Yue-Yu; Liu, Xusheng; Huang, Xiao‐Ru; Yu, Xueqing; Lan, Hui‐Yao

doi:10.3389/fcell.2020.00123

Cited by 152 publications

(109 citation statements)

References 152 publications

(156 reference statements)

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“…The SMAD family is composed of several TFs. SMAD3 is an important transporter in the transforming growth factor-β (TGF-β) signal transduction pathway, and SMAD7 has been considered as an important negative feedback regulator of the TGF-β signaling pathway in the past (114). It has been demonstrated that miR-497 directly interacts with the 3'-UTR sequence of SMAD3 transcripts, indicating that it may act as one of the regulators of the TGF-β signaling pathway (115).…”

Section: Mutual Regulation Of Mir-497 and Circular Rnas (Circrnas)mentioning

confidence: 99%

Regulation of microRNA‑497 expression in human cancer (Review)

Luo

Xia

et al. 2020

Oncol Lett

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Section: Mutual Regulation Of Mir-497 and Circular Rnas (Circrnas)mentioning

confidence: 99%

Regulation of microRNA‑497 expression in human cancer (Review)

Luo

Xia

et al. 2020

Oncol Lett

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“…TGF-β is a well-studied fibroblast-promoting factor and a powerful anti-inflammatory cytokine that regulates renal inflammation (54)(55)(56). It has been previously reported to modulate cell growth, differentiation and proliferation.…”

Section: Discussionmentioning

confidence: 99%

Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation

Wang

Wu²,

Dai

et al. 2020

Exp Ther Med

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Interstitial fibrosis is a typical feature of all progressive renal diseases. The process of fibrosis is frequently coupled with the presence of pro-fibrotic factors and inflammation. Naringin is a dihydroflavone compound that has been previously reported to exhibit anti-fibrotic effects in the liver, where it prevents oxidative damage. In the present study, a rat model of renal interstitial fibrosis and fibrosis cell model were established to evaluate the effects of naringin on inflammatory proteins and fibrosis markers in kidney of rats and NRK-52E cells, and to elucidate the role of the TGF-β/Smad signaling pathway in this mechanism. Compared with those in fibrotic NRK-52E cells that were stimulated by transforming growth factor-β (TGF-β), gene expression levels of α-smooth muscle actin (α-SMA), collagen 1 (COL1A1), collagen 3 (COL3A1), interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were all found to be significantly decreased in fibrotic NRK-52E cells following treatment with naringin (50, 100 and 200 ng/ml). Results from the histopathological studies showed that naringin treatment preserved the renal tissue structure and reduced the degree of fibrosis in the kidney tissues of rats that underwent unilateral ureteral obstruction (UUO). In addition, naringin administration reduced the expression of α-SMA, COL1A1, COL3A1, IL-1β, IL-6 and TNF-α in the kidneys of rats following UUO. The current study, using western blot analysis, indicated that naringin also downregulated the activation of Smad2/3 and the expression of Smad4, high-mobility group protein B1, activator protein-1, NF-κB and cyclooxygenase-2 whilst upregulating the expression of Smad7 in fibrotic NRK-52E cells and rats in the UUO group. In conclusion, naringin could antagonize renal interstitial fibrosis by regulating the TGF-β/Smad pathway and the expression of inflammatory factors.

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“…It is well-established that transforming growth factor β (TGF-β) as the master regulator for the fibrotic and inflammatory process in CKD ( Meng et al, 2016 ). Hyperglycemic factors such as advanced glycation end products (AGEs) and angiotensin II (AngII) may trigger the activation of TGF-β signaling via Smad dependent or independent pathway, therefore promoting fibrosis in kidneys ( Lan, 2011 ; Meng et al, 2016 ; Gu et al, 2020 ) ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

Huang

et al. 2021

Front. Pharmacol.

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Diabetic kidney disease (DKD) is the most common diabetic complication and is a leading cause of end-stage kidney disease. Increasing evidence shows that DKD is regulated not only by many classical signaling pathways but also by epigenetic mechanisms involving chromatin histone modifications, DNA methylation, and non-coding RNA (ncRNAs). In this review, we focus on our current understanding of the role and mechanisms of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the pathogenesis of DKD. Of them, the regulatory role of TGF-β/Smad3-dependent miRNAs and lncRNAs in DKD is highlighted. Importantly, miRNAs and lncRNAs as biomarkers and therapeutic targets for DKD are also described, and the perspective of ncRNAs as a novel therapeutic approach for combating diabetic nephropathy is also discussed.

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Diverse Role of TGF-β in Kidney Disease

Cited by 152 publications

References 152 publications

Regulation of microRNA‑497 expression in human cancer (Review)

Regulation of microRNA‑497 expression in human cancer (Review)

Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

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