lncRNA-Gm4419 alleviates renal damage in rats with diabetic nephropathy through NF-κB pathway

Li, Haizhen; Wu, Peipei; Sun, Dejing; Jiang, Lu; Yu, Jixiang; Wang, Cailing; Fan, Lei

doi:10.23736/s0031-0808.19.03844-8

Cited by 4 publications

(4 citation statements)

References 4 publications

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“…The overexpression of IL-18 and IL-1β facilitates fibrotic processes in the kidneys by promoting TGF-β activation in renal tubular epithelial cells, and ultimately resulting in the development and progression of DN (Tang and Yiu, 2020). The mechanism through which NLRP3 inflammasome causes DN is exceptionally complex, and LncRNAGm4419 has been implicated in glomerular thylakoid inflammation and fibrosis in hyperglycemic states via the NF-κB/ NLRP3 inflammatory pathway, which ultimately results in the development of DN (Li et al, 2020). In addition, previous studies have revealed that spleen tyrosine kinase (Syk) is involved in hyperglycemia-induced activation of the Syk/JNK/NLRP3 signaling pathway in rat glomerular thylakoid cells and HK2 cells.…”

Section: Discussionmentioning

confidence: 99%

Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome

Dong

Jia

et al. 2022

Front. Pharmacol.

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Diabetic nephropathy (DN) is one of the primary complications of diabetes. Fisetin is a flavonoid polyphenol that is present in several vegetables and fruits. The present study investigated the mechanisms of fisetin in DN-induced podocyte injury both in vitro and in vivo. The results revealed that fisetin ameliorated high glucose (HG)-induced podocyte injury and streptozotocin (STZ)-induced DN in mice. CDKN1B mRNA expression in the glomeruli of patients with DN decreased based on the Nephroseq dataset, and fisetin reversed CDKN1B expression at mRNA and protein levels in a dose-dependent manner in podocytes and mice kidney tissues. Furthermore, fisetin suppressed the phosphorylation of P70S6K, a downstream target of CDKN1B, activated autophagosome formation, and inhibited Nod-like receptor protein 3 (NLRP3) inflammasomes. Interfering CDKN1B reduced the protective effects of fisetin against high glucose-induced podocyte injury. Molecular docking results revealed a potential interaction between fisetin and CDKN1B. In summary, the present study revealed that fisetin alleviated high glucose-induced podocyte injury and STZ-induced DN in mice by restoring autophagy-mediated CDKN1B/P70S6K pathway and inhibiting NLRP3 inflammasome.

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Section: Discussionmentioning

confidence: 99%

Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome

Dong

Jia

et al. 2022

Front. Pharmacol.

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“…Through RNA sequencing and bioinformatics methods, it was found that lincRNA Gm4419 was the only factor that bound to NF-κB among 12 lncRNAs with abnormal DKD expression. It was further confirmed that knocking down Gm4419 in MCs cultured with high glucose could significantly improve inflammation, fibrosis and proliferation (Yi et al, 2017;Ma et al, 2019;Li et al, 2020a). Thus, lncRNA Gm4419 can improve the symptoms of diabetes and its complications by regulating the NF-κB signaling pathway and the ferroptosis pathway.…”

Section: Lncrnas Regulate Ferroptosis and Affect The Development Of D...mentioning

confidence: 91%

LncRNAs regulate ferroptosis to affect diabetes and its complications

et al. 2022

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Worldwide, the rapid increase in the incidence of diabetes and its complications poses a serious threat to human health. Ferroptosis, which is a new nonapoptotic form of cell death, has been proven to be closely related to the occurrence and development of diabetes and its complications. In recent years, lncRNAs have been confirmed to be involved in the occurrence and development of diabetes and play an important role in regulating ferroptosis. An increasing number of studies have shown that lncRNAs can affect the occurrence and development of diabetes and its complications by regulating ferroptosis. Therefore, lncRNAs have great potential as therapeutic targets for regulating ferroptosis-mediated diabetes and its complications. This paper reviewed the potential impact and regulatory mechanism of ferroptosis on diabetes and its complications, focusing on the effects of lncRNAs on the occurrence and development of ferroptosis-mediated diabetes and its complications and the regulation of ferroptosis-inducing reactive oxygen species, the key ferroptosis regulator Nrf2 and the NF-κB signaling pathway to provide new therapeutic strategies for the development of lncRNA-regulated ferroptosis-targeted drugs to treat diabetes.

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“…68 Gm4419 (Ensembl ID ENSMUST00000180671), a regulator of the NF-κB signalling pathway located on chromosome 12, has been reported to attenuate renal injury in DKD rats through the NF-κB signalling pathway. 69 Gm4419 is overexpressed in renal tissues of DKD mice and HMCs and directly interacts with the p50 subunit of NF-κB thereby activating the NF-κB/NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory vesicle signalling pathway, promoting the release of inflammatory cytokines and increasing the expression of renal fibrosis markers. 70 Growth arrest-specific transcript 5 (GAS5) was originally discovered in a study designed to screen for genes specifically expressed during growth arrest in mammalian cells.…”

Section: Other Lncrnas With Expression In MCmentioning

confidence: 99%

“…MIAT expression is upregulated in the DKD and releases E2F transcription factor 3 (E2F3) through competitive binding with miR‐147a, thereby inducing cell proliferation, ECM accumulation, and fibrosis in MCs 68 . Gm4419 (Ensembl ID ENSMUST00000180671), a regulator of the NF‐κB signalling pathway located on chromosome 12, has been reported to attenuate renal injury in DKD rats through the NF‐κB signalling pathway 69 . Gm4419 is overexpressed in renal tissues of DKD mice and HMCs and directly interacts with the p50 subunit of NF‐κB thereby activating the NF‐κB/NOD‐like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory vesicle signalling pathway, promoting the release of inflammatory cytokines and increasing the expression of renal fibrosis markers 70 .…”

Section: Lncrnas Affect Various Pathologic Changes In Dkdmentioning

confidence: 99%

The role of long non‐coding RNAs in the development of diabetic kidney disease and the involved clinical application

Hou,

2024

Diabetes Metabolism Res

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Diabetic kidney disease (DKD), one of the common microvascular complications of diabetes, is increasing in prevalence worldwide and can lead to End‐stage renal disease. However, there are still gaps in our understanding of the pathophysiology of DKD, and both current clinical diagnostic methods and treatment strategies have drawbacks. According to recent research, long non‐coding RNAs (lncRNAs) are intimately linked to the developmental process of DKD and could be viable targets for clinical diagnostic decisions and therapeutic interventions. Here, we review recent insights gained into lncRNAs in pathological changes of DKD such as mesangial expansion, podocyte injury, renal tubular injury, and interstitial fibrosis. We also discuss the clinical applications of DKD‐associated lncRNAs as diagnostic biomarkers and therapeutic targets, as well as their limitations and challenges, to provide new methods for the prevention, diagnosis, and treatment of DKD.

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lncRNA-Gm4419 alleviates renal damage in rats with diabetic nephropathy through NF-κB pathway

Cited by 4 publications

References 4 publications

Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome

Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome

LncRNAs regulate ferroptosis to affect diabetes and its complications

The role of long non‐coding RNAs in the development of diabetic kidney disease and the involved clinical application

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