Long non-coding RNAs: A double-edged sword in aging kidney and renal disease

Wang, Yanni; Yang, Change; Zhang, Dandan; Chen, Yuanyuan; Yu, Xiao; Yan, Zhao; Miao, Hua

doi:10.1016/j.cbi.2021.109396

Cited by 13 publications

(9 citation statements)

References 168 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Long noncoding RNA is a well-known endogenous noncoding RNA (200 nucleotides long) [4]. LncRNAs regulate gene expression by taking part in physiological processes, including nuclear transport, alternative splicing, and epigenetics [5].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA ZFAS1 Protects HK-2 Cells against Sepsis‐Induced Injury through Targeting the miR3723p/PPARα Axis

Hei

Yue

Sun

2022

Journal of Healthcare Engineering

View full text Add to dashboard Cite

In septic acute kidney injury, one of the main purposes of long noncoding RNA (lncRNA) ZFAS1 is still unclear. This study is intended to analyze the effects of lncRNA ZFAS1 on the septic AKI in the HK-2 cell line. Materials and Methods. In order to construct an in vitro model of septic AKI, HK-2 cells have been treated with lipopolysaccharides. CCK-8 assay has been utilized to check the viability of HK-2 cells. The contents of inflammatory cytokines (that includes IL-1β, TNF-α, and IL-6) have been marked with enzyme-linked immune sorbent assay (ELISA). Cell apoptosis was assessed by TUNEL staining. To detect the expression of lncRNA ZFAS1 and microRNA-372-3p, quantitative reverse-transcription PCR has been used. And to confirm the connection among genes, luciferase reporter assay has been applied. Results. Overexpression of ZFAS1 alleviated LPS‐induced HK-2 cell injury. ZFAS1 positively regulated expression of α receptor activated by peroxisome proliferation (PPARα) through competitive linkage with miR-372-3p. In addition, over expression of miR-372-3p counteracted the protective effect of upward regulation of ZFAS1 on LPS-induced HK-2 cell damage, which could be reversed by over expression of PPARα. Conclusion. It is concluded that, in LPS-induced HK-2 cell injury, ZFAS1 has a protective role via modulating the miR-372-3p/PPARα axis, suggesting the potential of ZFAS1 as a protective target for septic AKI.

show abstract

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA ZFAS1 Protects HK-2 Cells against Sepsis‐Induced Injury through Targeting the miR3723p/PPARα Axis

Hei

Yue

Sun

2022

Journal of Healthcare Engineering

View full text Add to dashboard Cite

show abstract

“…The progression of CKD and renal fibrosis, one of the biggest issues in nephrology, indicated that patients inevitably progress ESRD and require dialysis or kidney transplantation ( Webster et al, 2017 ; Aydin et al, 2019 ; Van Sandwijk et al, 2019 ). Numerous studies have demonstrated that renal fibrosis was associated with the dysbiosis or dysregulation of gut microbiota, non-coding RNAs, renin–angiotensin system, aryl hydrocarbon receptor, IƙB/NF-ƙB, Keap1/Nrf2, TGF-β/Smad, and Wnt/β-catenin signaling pathways ( Ma et al, 2018a ; Chen et al, 2019b ; Garg and Maurya, 2019 ; Zhao et al, 2019 ; Hu et al, 2020a ; Miao et al, 2021b ; Wang et al, 2021d ; Wu et al, 2021 ; Zhou et al, 2021 ) as well as metabolite disorders including tryptophan metabolism and lipid metabolism ( Zhao, 2013a ; Zhao et al, 2015 ; Wang et al, 2019 ; Liu et al, 2021a ). Further studies have demonstrated that activation of IƙB/NF-ƙB and Keap1/Nrf2 signaling pathways could mediate or crosstalk these signaling pathways in both patients with CKD and experimental research studies ( Chen et al, 2017a ; Chen et al, 2017b ; Chen et al, 2019c ).…”

Section: Discussionmentioning

confidence: 99%

Shenkang Injection and Its Three Anthraquinones Ameliorates Renal Fibrosis by Simultaneous Targeting IƙB/NF-ƙB and Keap1/Nrf2 Signaling Pathways

Luo

Suo²,

Ren³

et al. 2021

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Oxidative stress and inflammation are important and critical mediators in the development and progression of chronic kidney disease (CKD) and its complications. Shenkang injection (SKI) has been widely used to treat patients with CKD. Although the anti-oxidative and anti-inflammatory activity was involved in SKI against CKD, its bioactive components and underlying mechanism remain enigmatic. A rat model of adenine-induced chronic renal failure (CRF) is associated with, and largely driven by, oxidative stress and inflammation. Hence, we identified the anti-oxidative and anti-inflammatory components of SKI and further revealed their underlying mechanism in the adenine-induced CRF rats. Compared with control rats, the levels of creatinine, urea, uric acid, total cholesterol, triglyceride, and low-density lipoprotein cholesterol in serum were significantly increased in the adenine-induced CRF rats. However, treatment with SKI and its three anthraquinones including chrysophanol, emodin, and rhein could reverse these aberrant changes. They could significantly inhibit pro-fibrotic protein expressions including collagen I, α-SMA, fibronectin, and vimentin in the kidney tissues of the adenine-induced CRF rats. Of note, SKI and rhein showed the stronger inhibitory effect on these pro-fibrotic protein expressions than chrysophanol and emodin. Furthermore, they could improve dysregulation of IƙB/NF-ƙB and Keap1/Nrf2 signaling pathways. Chrysophanol and emodin showed the stronger inhibitory effect on the NF-κB p65 protein expression than SKI and rhein. Rhein showed the strongest inhibitory effect on p65 downstream target gene products including NAD(P)H oxidase subunits (p47phox, p67phox, and gp91phox) and COX-2, MCP-1, iNOS, and 12-LO in the kidney tissues. However, SKI and rhein showed the stronger inhibitory effect on the significantly downregulated anti-inflammatory and anti-oxidative protein expression nuclear Nrf2 and its target gene products including HO-1, catalase, GCLC, and NQO1 in the Keap1/Nrf2 signaling pathway than chrysophanol and emodin. This study first demonstrated that SKI and its major components protected against renal fibrosis by inhibiting oxidative stress and inflammation via simultaneous targeting IƙB/NF-ƙB and Keap1/Nrf2 signaling pathways, which illuminated the potential molecular mechanism of anti-oxidative and anti-inflammatory effects of SKI.

show abstract

“…Long non-coding RNAs (lncRNAs) are an emerging class of non-coding RNAs, which are more than 200 nucleotides in length ( Luo et al, 2020 ; Wang et al, 2021b ). lncRNAs can regulate various biological functions at epigenetic, transcriptional and post-transcriptional levels ( Huang, 2018 ) and bind DNA, RNA and protein ( Wang Y.-N. et al, 2021 ). Mechanism studies have shown that TGF-β1/Smad3 is able to promote renal inflammation and fibrosis by regulating lncRNAs ( Tang et al, 2017 ).…”

Section: Crosstalk Between Tgf-β1/smad and Long Non-coding Rna In Tub...mentioning

confidence: 99%

TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis

Sun

Zhang

et al. 2022

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Chronic kidney disease (CKD) was a major public health problem worldwide. Renal fibrosis, especially tubulointerstitial fibrosis, is final manifestation of CKD. Many studies have demonstrated that TGF-β/Smad signaling pathway plays a crucial role in renal fibrosis. Therefore, targeted inhibition of TGF-β/Smad signaling pathway can be used as a potential therapeutic measure for tubulointerstitial fibrosis. At present, a variety of targeting TGF-β1 and its downstream Smad proteins have attracted attention. Natural products used as potential therapeutic strategies for tubulointerstitial fibrosis have the characteristics of acting on multiple targets by multiple components and few side effects. With the continuous research and technique development, more and more molecular mechanisms of natural products have been revealed, and there are many natural products that inhibited tubulointerstitial fibrosis via TGF-β/Smad signaling pathway. This review summarized the role of TGF-β/Smad signaling pathway in tubulointerstitial fibrosis and natural products against tubulointerstitial fibrosis by targeting TGF-β/Smad signaling pathway. Additionally, many challenges and opportunities are presented for inhibiting renal fibrosis in the future.

show abstract

Long non-coding RNAs: A double-edged sword in aging kidney and renal disease

Cited by 13 publications

References 168 publications

Long Noncoding RNA ZFAS1 Protects HK-2 Cells against Sepsis‐Induced Injury through Targeting the miR3723p/PPARα Axis

Long Noncoding RNA ZFAS1 Protects HK-2 Cells against Sepsis‐Induced Injury through Targeting the miR3723p/PPARα Axis

Shenkang Injection and Its Three Anthraquinones Ameliorates Renal Fibrosis by Simultaneous Targeting IƙB/NF-ƙB and Keap1/Nrf2 Signaling Pathways

TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis

Contact Info

Product

Resources

About