MicroRNA-214 promotes chronic kidney disease by disrupting mitochondrial oxidative phosphorylation

Bai, Mei; Chen, Huimei; Ding, Dan; Song, Rongfang; Lin, Jiajuan; Zhang, Yuanyuan; Guo, Yan; Chen, Shuang; Ding, Guofu; Zhang, Yue; Jia, Zhanjun; Huang, Songming; He, John Cijiang; Yang, Li; Zhang, Aihua

doi:10.1016/j.kint.2018.12.028

Cited by 73 publications

(40 citation statements)

References 39 publications

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“…In this regard, an obvious but challenging question moving forward is whether drugs such as miRNA mimics designed to further enhance miR-214 activity are beneficial in ADPKD. Similar to our findings, miR-214 expression is increased in mouse models of acute kidney injury and fibrosis (34)(35)(36). However, miR-214 appears to produce divergent effects in kidney injury models.…”

Section: Discussionsupporting

confidence: 90%

Interstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progression

et al. 2020

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Section: Discussionsupporting

confidence: 90%

Interstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progression

et al. 2020

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“…DOI 10.1002/em PNPase or AGO2 may be involved with the transport process (Wang et al, 2010;Bandiera et al, 2011;Zhang et al, 2014;Shepherd et al, 2017). Another mitomiR, miR-214, has been implicated in the pathogenesis of chronic kidney disease (CKD) by disrupting OXPHOS due to downregulation of MT-ND4L and MT-ND6 and is suggested to be a potential therapeutic target and biomarker for CKD (Bai et al, 2019). mitomiRs can enhance or repress protein expression at both transcriptional and translational levels resulting in the modulation of mitochondrial metabolic activity and cellular homeostasis.…”

Section: Small Noncoding Rnasmentioning

confidence: 99%

“…Similarly, miR-378 overexpression in Type I diabetes downregulates the mitochondrial encoded F0 component MT-ATP6 (Jagannathan et al, 2015). Another mitomiR, miR-214, has been implicated in the pathogenesis of chronic kidney disease (CKD) by disrupting OXPHOS due to downregulation of MT-ND4L and MT-ND6 and is suggested to be a potential therapeutic target and biomarker for CKD (Bai et al, 2019).…”

Section: Small Noncoding Rnasmentioning

confidence: 99%

Mitochondrial DNA: Epigenetics and environment

Sharma

Pasala

Prakash

2019

Environ and Mol Mutagen

120

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Maintenance of the mitochondrial genome is essential for proper cellular function. For this purpose, mitochondrial DNA (mtDNA) needs to be faithfully replicated, transcribed, translated, and repaired in the face of constant onslaught from endogenous and environmental agents. Although only 13 polypeptides are encoded within mtDNA, the mitochondrial proteome comprises over 1500 proteins that are encoded by nuclear genes and translocated to the mitochondria for the purpose of maintaining mitochondrial function. Regulation of mtDNA and mitochondrial proteins by epigenetic changes and post‐translational modifications facilitate crosstalk between the nucleus and the mitochondria and ultimately lead to the maintenance of cellular health and homeostasis. DNA methyl transferases have been identified in the mitochondria implicating that methylation occurs within this organelle; however, the extent to which mtDNA is methylated has been debated for many years. Mechanisms of demethylation within this organelle have also been postulated, but the exact mechanisms and their outcomes is still an active area of research. Mitochondrial dysfunction in the form of altered gene expression and ATP production, resulting from epigenetic changes, can lead to various conditions including aging‐related neurodegenerative disorders, altered metabolism, changes in circadian rhythm, and cancer. Here, we provide an overview of the epigenetic regulation of mtDNA via methylation, long and short noncoding RNAs, and post‐translational modifications of nucleoid proteins (as mitochondria lack histones). We also highlight the influence of xenobiotics such as airborne environmental pollutants, contamination from heavy metals, and therapeutic drugs on mtDNA methylation. Environ. Mol. Mutagen., 60:668–682, 2019. © 2019 Wiley Periodicals, Inc.

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“…It is noticeable that the regulatory function of miR-214 in inflammatory response has been demonstrated, and it is determined as one of the key molecules that serve as potential therapeutic targets in inflammation-associated diseases [17]. Subsequent studies have confirmed the close relationship of miR-214 with inflammatory response in some diseases [18,19]. Considering the pivotal role of DPP4 and inflammation in the development of IR, we deduced that miR-214 might also be associated with obesityinduced IR.…”

Section: Introductionmentioning

confidence: 81%

“…miR-214 has previously reported to be deregulated in hepatic IR [15] and muscle cell IR [33], and it is determined as a key molecule in the regulation of inflammation [17][18][19], but rare evidence for its role in obesityinduced IR. In this study, the expression of miR-214 in obese patients with IR was estimated and its clinical value in diagnosis was further evaluated.…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of miR-214 is associated with obesity-induced insulin resistance as a biomarker and therapeutic

Cheng

Yuan

et al. 2020

Diagn Pathol

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Background: Insulin resistance (IR) in obesity is associated with the occurrence of metabolic and cardiovascular diseases. Dipepidyl peptidase 4 (DPP4) plays a pivotal role during the development of IR, and was found to be a target gene of microRNA-214 (miR-214) in our study. This study sought to assess the expression and clinical value of miR-214 in obese patients with IR, and investigate its therapeutic potential in obese rats and adipocytes with IR. Methods: Serum expression of miR-214 in obese patients with or without IR was estimated by quantitative realtime-PCR. A receiver operating characteristic curve was plotted to evaluate the diagnostic value of miR-214 in the patients. Obesity-induced IR animal and cell models were constructed, and the therapeutic ability of miR-214 was explored. Results: Serum expression of miR-214 was decreased in obese patients compared with the healthy controls, and the lowest expression was observed in the cases with IR. Downregulation of miR-214 was significantly correlated with the serum DPP4 levels and HOMA-IR of the patients upon IR conditions, and was demonstrated to perform diagnostic accuracy for distinguishing obese patients with IR from those without IR. In obesity-associated IR animal and cell models, the downregulation of miR-214 was also been detected. According to the measurement of glucose and insulin tolerance and glucose uptake abilities, we found that the overexpression of miR-214 could be used to alleviate IR in the IR models, especially when collaboratively used with DPP4 inhibitor vildagliptin. Conclusion: All data revealed that miR-214, as a regulator of DPP4, is decreased in obese patients with IR and may serve as a diagnostic biomarker. The upregulation of miR-214 could improve IR in obese rats and adipocytes, indicating that miR-214 has the therapeutic potential for obesity and IR.

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MicroRNA-214 promotes chronic kidney disease by disrupting mitochondrial oxidative phosphorylation

Cited by 73 publications

References 39 publications

Interstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progression

Interstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progression

Mitochondrial DNA: Epigenetics and environment

Aberrant expression of miR-214 is associated with obesity-induced insulin resistance as a biomarker and therapeutic

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