Data of expression status of miR- 29a and its putative target mitochondrial apoptosis regulatory gene DRP1 upon miR-15a and miR-214 inhibition

Jan, Muhammad Ishtiaq; Khan, Riaz A.; Malik, Abdul; Ali, Tahir; Bilal, Muhammad; Long, Bo; Sajid, Abdul; Urehman, Naseeb; Waseem, Nayyar; Nawab, Javed; Ali, Murad; Majeed, Abdul; Ahmad, Hamid; Aslam, Sohail; Hamera, Sadia; Sultan, Aneesa; Aneesa, Mariam; Javed, Qamar; Murtaza, Iram

doi:10.1016/j.dib.2017.12.040

Cited by 8 publications

(3 citation statements)

References 9 publications

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“…MiR-29a protects mitochondrial structural integrity, restricts mito-DAMPs, and exerts an anti-inflammatory effect on the pathogenesis of NAFLD by targeting voltage-dependent anion channels and Bcl-2-associated X genes, whose oligomerization is involved in mPTP opening and mito-DAMPs release [193,194]. One computational analysis revealed that miR-29a targeted DRP1 [195], which suggests its potential role in regulating mitochondrial dynamics and mitophagy. MiR-29a inhibits glycogen synthase kinase-3β (GSK3β) to suppress sirtuin 1 (SIRT1)-mediated mitochondrial biogenesis, which leads to alleviation of mitochondrial proteostatic stress and UPRmt in the context of NASH [196].…”

Section: Mitochondrial Micrornas Interferencementioning

confidence: 99%

Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

Xie

Song

et al. 2022

Acta Pharmacol Sin

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Mitochondrial biology and behavior are central to the physiology of liver. Multiple mitochondrial quality control mechanisms remodel mitochondrial homeostasis under physiological and pathological conditions. Mitochondrial dysfunction and damage induced by overnutrition lead to oxidative stress, inflammation, liver cell death, and collagen production, which advance hepatic steatosis to nonalcoholic steatohepatitis (NASH). Accumulating evidence suggests that specific interventions that target mitochondrial homeostasis, including energy metabolism, antioxidant effects, and mitochondrial quality control, have emerged as promising strategies for NASH treatment. However, clinical translation of these findings is challenging due to the complex and unclear mechanisms of mitochondrial homeostasis in the pathophysiology of NASH.

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Section: Mitochondrial Micrornas Interferencementioning

confidence: 99%

Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

Xie

Song

et al. 2022

Acta Pharmacol Sin

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“…Drp1 has been shown to be the target of several miRNAs including miR411, miR29a, and miR150–5p. ( Jan et al, 2018 ; Wang Z. J. et al, 2021 ; Yang W et al, 2021 ). MiRs-34 belongs to mitomiRs, consistent with the results in our study, but its role in mitochondrial function is not completely understood ( Barrey et al, 2011 ; Geiger and Dalgaard, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

The effect of a traditional Chinese quadri-combination therapy and its component quercetin on recurrent spontaneous abortion: A clinical trial, network pharmacology and experiments-based study

Zhou

Li²,

Pan³

et al. 2022

Front. Pharmacol.

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Objective: To explore the effect and mechanisms of a traditional Chinese quadri-combination therapy [Bushen, Yiqi, Lixue and Yangtai (BYLY)] in treating recurrent spontaneous abortion (RSA).Methods: A clinical trial was conducted to study the effect of BYLY on RSA. Pharmacological network analysis and UPLC-Q/TOF-mass spectrometry (MS) were applied to investigate the key active component in BYLY and potential targets. Cellular experiments based on former results were performed to examine the mechanism of BYLY in the treatment of RSA.Results: Four hundred and eighty participants enrolled in the clinical trial. The results showed that, compared with the use of BYLY or duphaston alone, a combination of duphaston and BYLY could decrease the early abortion rate in RSA (p < 0.001). Network pharmacological analysis indicated that BYLY contained 132 active components and 146 core targets, and the quercetin maybe the key effective component. In vitro experiments found that pretreatment of quercetin at the correct concentration (2 μM) prevented hypoxia-induced viability and proliferation reduction, and apoptosis and mitochondrial dysfunction. Furthermore, quercetin could modulate mitochondrial fission/fusion balance in trophoblasts, and specifically decrease the expression of Drp1 by regulating miR-34a-5p.Conclusion: BYLY could improve pregnancy outcomes of RSA, based on multi-components and multi-targets. The protective effect of quercetin on trophoblasts, through decreasing Drp1 expression via regulating miR-34a-5p, might be one possible effective mechanism.

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“…The p53 upregulated modulator of apoptosis (PUMA), an activator of BAX/BAK for the induction of MPT and subsequent apoptosis, can also be targeted by miR-29a [134]. Moreover, one computational analysis revealed that miR-29a targets dynamin-related protein 1 (DRP1) [135], implying its potential role in regulating mitochondrial dynamics and mitophagy. In line with the aforementioned studies, our experimental results have shown that liver protective-miR-29a can reduce BAX expression [46].…”

Section: Role Of Mir-29a In Mitochondrial Metabolismmentioning

confidence: 99%

The Emerging Role of MicroRNAs in NAFLD: Highlight of MicroRNA-29a in Modulating Oxidative Stress, Inflammation, and Beyond

Lin

Yang

Wang

et al. 2020

Cells

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Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease and ranges from steatosis to steatohepatitis and to liver fibrosis. Lipotoxicity in hepatocytes, elevated oxidative stress and the activation of proinflammatory mediators of Kupffer cells, and fibrogenic pathways of activated hepatic stellate cells can contribute to the development of NAFLD. MicroRNAs (miRs) play a crucial role in the dysregulated metabolism and inflammatory signaling connected with NAFLD and its progression towards more severe stages. Of note, the protective effect of non-coding miR-29a on liver damage and its versatile action on epigenetic activity, mitochondrial homeostasis and immunomodulation may improve our perception of the pathogenesis of NAFLD. Herein, we review the biological functions of critical miRs in NAFLD, as well as highlight the emerging role of miR-29a in therapeutic application and the recent advances in molecular mechanisms underlying its liver protective effect.

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Data of expression status of miR- 29a and its putative target mitochondrial apoptosis regulatory gene DRP1 upon miR-15a and miR-214 inhibition

Cited by 8 publications

References 9 publications

Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

The effect of a traditional Chinese quadri-combination therapy and its component quercetin on recurrent spontaneous abortion: A clinical trial, network pharmacology and experiments-based study

The Emerging Role of MicroRNAs in NAFLD: Highlight of MicroRNA-29a in Modulating Oxidative Stress, Inflammation, and Beyond

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