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学者姓名:刘健康

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Preface Scopus SCIE
其他 | 2022 , 193 , 58-58
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[无可用摘要]

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GB/T 7714 Liu, J. , Wallace, D.C. . Preface [未知].
MLA Liu, J. 等. "Preface" [未知].
APA Liu, J. , Wallace, D.C. . Preface [未知].
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Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changes via modulation of mitochondrial homeostasis EI SCIE Scopus
期刊论文 | 2022 , 13 (16) , 8676-8684 | FOOD & FUNCTION
SCOPUS Cited Count: 2
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Strenuous exercise is reported to provoke deleterious consequences including cardiac impairments, while the detailed mechanisms and effective interventions remain limited. The current study aims to explore the profitable effects of hydroxytyrosol (HT), one of the most abundant polyphenols derived from olive oil, on strenuous exercise-induced pathological changes in the heart and its underlying mechanisms. Sprague-Dawley male rats at the age of 8-week-old were supplemented with 25 mg kg(-1) day(-1) of HT 45 min before the beginning of strenuous exercise for a total of 8 weeks. HT treatment obviously improved the heart weight and morphology with lowered serum cardiac hypertrophy markers as well as cardiac oxidative stress. Moreover, the down-regulated mitochondrial biogenesis pathway, impaired mitochondrial complex activity, dysregulated expression of mitochondrial dynamics-related proteins and activated apoptotic pathway induced by Exe were all improved by HT. In vitro, 10 mu M HT effectively reduced the reactive oxygen species level, promoted mitochondrial biogenesis, and inhibited apoptosis and cardiomyocyte hypertrophy in an angiotensin II-induced cardiomyocyte hypertrophy model. In addition, knockdown of the peroxisome proliferator-activated receptor gamma coactivator-1 alpha, the key regulator of mitochondrial biogenesis, partially abolished the benefits of HT. Our results demonstrate that the disturbance of mitochondrial homeostasis plays a substantial role in strenuous exercise-induced pathological cardiac hypertrophy, and HT presents as an effective intervention strategy targeting mitochondrial homeostasis for cardiac health.

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GB/T 7714 Xiong, Yue , Xu, Jie , Cao, Wenli et al. Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changes via modulation of mitochondrial homeostasis [J]. | FOOD & FUNCTION , 2022 , 13 (16) : 8676-8684 .
MLA Xiong, Yue et al. "Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changes via modulation of mitochondrial homeostasis" . | FOOD & FUNCTION 13 . 16 (2022) : 8676-8684 .
APA Xiong, Yue , Xu, Jie , Cao, Wenli , Zhang, Jiawei , Feng, Zhihui , Cao, Ke et al. Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changes via modulation of mitochondrial homeostasis . | FOOD & FUNCTION , 2022 , 13 (16) , 8676-8684 .
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Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy SCIE Scopus
期刊论文 | 2022 , 13 (1) | NATURE COMMUNICATIONS
SCOPUS Cited Count: 16
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Functional succinate dehydrogenase (SDH) complex is vital to mitochondrial homeostasis. Here the authors show that disruption of SDH assembly in the heart causes dilated cardiomyopathy via impairing the mitochondrial integrity and metabolism and that mitochondrial interventions can be an effective approach to ameliorate the disease progression. Succinate dehydrogenase, which is known as mitochondrial complex II, has proven to be a fascinating machinery, attracting renewed and increased interest in its involvement in human diseases. Herein, we find that succinate dehydrogenase assembly factor 4 (SDHAF4) is downregulated in cardiac muscle in response to pathological stresses and in diseased hearts from human patients. Cardiac loss of Sdhaf4 suppresses complex II assembly and results in subunit degradation and complex II deficiency in fetal mice. These defects are exacerbated in young adults with globally impaired metabolic capacity and activation of dynamin-related protein 1, which induces excess mitochondrial fission and mitophagy, thereby causing progressive dilated cardiomyopathy and lethal heart failure in animals. Targeting mitochondria via supplementation with fumarate or inhibiting mitochondrial fission improves mitochondrial dynamics, partially restores cardiac function and prolongs the lifespan of mutant mice. Moreover, the addition of fumarate is found to dramatically improve cardiac function in myocardial infarction mice. These findings reveal a vital role for complex II assembly in the development of dilated cardiomyopathy and provide additional insights into therapeutic interventions for heart diseases.

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GB/T 7714 Wang, Xueqiang , Zhang, Xing , Cao, Ke et al. Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy [J]. | NATURE COMMUNICATIONS , 2022 , 13 (1) .
MLA Wang, Xueqiang et al. "Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy" . | NATURE COMMUNICATIONS 13 . 1 (2022) .
APA Wang, Xueqiang , Zhang, Xing , Cao, Ke , Zeng, Mengqi , Fu, Xuyang , Zheng, Adi et al. Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy . | NATURE COMMUNICATIONS , 2022 , 13 (1) .
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Daphnetin ameliorates A? pathogenesis via STAT3/GFAP signaling in an APP/PS1 double-transgenic mouse model of Alzheimer?s disease SCIE Scopus
期刊论文 | 2022 , 180 | PHARMACOLOGICAL RESEARCH
SCOPUS Cited Count: 10
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Alzheimer's disease (AD) has become a major public health problem that affects the elderly population. Therapeutic compounds with curative effects are not available due to the complex pathogenesis of AD. Daphnetin, a natural coumarin derivative and inhibitor of various kinases, has anti-inflammatory and antioxidant activities. In this study, we found that daphnetin improved spatial learning and memory in an amyloid precursor protein (APP)/presenilin 1 (PS1) double-transgenic mouse model of AD. Daphnetin markedly decreased the levels of amyloid-beta peptide 1-40 (A beta 40) and 1-42 (A beta 42) in the cerebral cortex, downregulated the expressions of enzymes involved in APP processing, e.g., beta-site APP-cleaving enzyme (BACE), nicastrin and presenilin enhancer protein 2 (PEN2). We further found the reduced serum levels of inflammatory factors, including interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and chemokine (C-C motif) ligand 3 (CCL3), while daphnetin increased total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) levels in the serum. Interestingly, daphnetin markedly decreased the expression of glial fibrillary acidic protein (GFAP) and the upstream regulatory molecule- phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in APP/PS1 mice, and mainly inhibited the phosphorylation of STAT3 at Ser727 to decrease GFAP expression evidenced in a LPS-activated glial cell model. These results suggest that daphnetin ameliorates cognitive deficits and that A beta deposition in APP/PS1 mice is mainly correlated with astrocyte activation and APP processing.

Keyword :

A? AD Astrocyte Daphnetin GFAP p-STAT3

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GB/T 7714 Gao, Peipei , Wang, Zhen , Lei, Mengyao et al. Daphnetin ameliorates A? pathogenesis via STAT3/GFAP signaling in an APP/PS1 double-transgenic mouse model of Alzheimer?s disease [J]. | PHARMACOLOGICAL RESEARCH , 2022 , 180 .
MLA Gao, Peipei et al. "Daphnetin ameliorates A? pathogenesis via STAT3/GFAP signaling in an APP/PS1 double-transgenic mouse model of Alzheimer?s disease" . | PHARMACOLOGICAL RESEARCH 180 (2022) .
APA Gao, Peipei , Wang, Zhen , Lei, Mengyao , Che, Jiaxing , Zhang, Shuangxi , Zhang, Tiantian et al. Daphnetin ameliorates A? pathogenesis via STAT3/GFAP signaling in an APP/PS1 double-transgenic mouse model of Alzheimer?s disease . | PHARMACOLOGICAL RESEARCH , 2022 , 180 .
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Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells EI SCIE PubMed
期刊论文 | 2021 , 13 (37) , 15928-15936 | NANOSCALE
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In the last decade, breakthroughs in liquid-phase transmission electron microscopy (TEM) have enabled in situ visualization of the motion dynamics of nanostructures in liquid media with unprecedented detail. However, it remains a significant challenge to perform liquid-phase TEM due to the intricate preparation procedure of liquid cells to keep liquid from evaporating under ultrahigh vacuum conditions in TEM columns. In the present study, the nonvolatility and remarkable solvation property of ionic liquids (ILs) is exploited to image the dynamic processes of DNA supramolecular aggregates and Au nanoparticle (NP) aggregates encompassing Brownian motions, interactions among individual nanoobjects and changes in architecture at nanometer resolution. Significant differences in motion behaviors are observed between DNA supramolecular aggregates and Au NP aggregates. Moreover, the temperature and dose dependence of dynamic motions are also investigated. The findings provide insights into the dynamics of DNA supramolecular aggregates and Au NP aggregates in ILs and present an easily accessible approach for probing the dynamic processes of biomacromolecular and other soft matter aggregates with various kinds of ILs at the nanoscale level.

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GB/T 7714 Lu, Zhuoyang , Liu, Xiangyang , He, Maogang et al. Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells [J]. | NANOSCALE , 2021 , 13 (37) : 15928-15936 .
MLA Lu, Zhuoyang et al. "Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells" . | NANOSCALE 13 . 37 (2021) : 15928-15936 .
APA Lu, Zhuoyang , Liu, Xiangyang , He, Maogang , Long, Jiangang , Liu, Jiankang . Dynamic motions and architectural changes in DNA supramolecular aggregates visualized via transmission electron microscopy without liquid cells . | NANOSCALE , 2021 , 13 (37) , 15928-15936 .
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Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia SCIE PubMed
期刊论文 | 2021 , 14 , 2851-2863 | JOURNAL OF INFLAMMATION RESEARCH
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Background: Microglia play an essential role in the central nervous system immune response. The transcription factor myocyte enhancer factor-2 D (MEF2D) is known to participate in stress regulation in various cell types and is easily activated in microglia. MEF2D has been shown to transcriptionally regulate several cytokine genes in immune cells and directly regulates the inflammatory response, suggesting that MEF2D may act as a key stimulus response regulator of microglia and is involved in the regulation of brain micro-homeostasis. To uncover the molecular mechanism of MEF2D in the inflammatory system, in the present study, we investigated the global effect of MEF2D in activated microglia and explored its potential regulatory network. Methods: Experiments with a recombinant lentiviral vector containing either shRNA or overexpressing MEF2D were performed in the murine microglial BV2 cell line. Transcriptome sequencing and global gene expression patterns were analysed in lipopoly-saccharide-stimulated shMEF2D BV2 cells. Pro-and anti-inflammatory factors were assessed by Western blot, qPCR or ELISA, and microglial activity was assessed by phago-cytosis and morphologic analysis. The direct binding of MEF2D to the promoter region of interferon regulatory factor 7 (IRF7) was tested by ChIP-qPCR. The interferon-stimulated genes (ISGs) were tested by qPCR. Results: MEF2D actively participated in the inflammatory response of BV2 microglial cells. Stably expressed RNAi-induced silencing of MEF2D disrupted the microglial immune balance in two ways: (1) the expression of proinflammatory factors, such as NLRP3, IL-1 beta, and iNOS was promoted; and (2) the type-I interferon signalling pathway was markedly inhibited by directly modulating IRF7 transcription. In contrast, overexpression of MEF2D significantly reduced the expression of NLRP3 and iNOS under LPS stimulation and alleviated the level of immune stress in microglia. Conclusion: These findings demonstrate that MEF2D plays an important role in regulating inflammatory homeostasis partly through transcriptional regulation of the type-I interferon signalling pathway.

Keyword :

inflammatory homeostasis IRF7 MEF2D microglia type-I interferons

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GB/T 7714 Lu, Fangfang , Wang, Ronglin , Xia, Li et al. Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia [J]. | JOURNAL OF INFLAMMATION RESEARCH , 2021 , 14 : 2851-2863 .
MLA Lu, Fangfang et al. "Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia" . | JOURNAL OF INFLAMMATION RESEARCH 14 (2021) : 2851-2863 .
APA Lu, Fangfang , Wang, Ronglin , Xia, Li , Nie, Tiejian , Gao, Fei , Yang, Shaosong et al. Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia . | JOURNAL OF INFLAMMATION RESEARCH , 2021 , 14 , 2851-2863 .
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LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells SCIE PubMed
期刊论文 | 2021 , 81 (11) , 2918-2929 | CANCER RESEARCH
WoS CC Cited Count: 3
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The long noncoding RNA (lncRNA) SAMMSON is required for human melanoma cell growth and survival. However, whether SAMMSON regulates the response of mutant BRAF melanoma cells to RAF inhibitors remains unknown. In this work, we showed that SAMMSON is rapidly induced upon inhibition of ERK signaling, and SAMMSON overexpression conferred resistance to vemurafenib-induced cytotoxicity in melanoma cells. SOX10 mediated transcriptional induction of SAMMSON by vemurafenib, and SOX10 sumoylation at K55 was essential for this function. In addition, depletion of SAMMSON activated p53 signaling, which is dependent on the SAMMSON-interacting protein CARF. Depletion of SAMMSON sensitized mutant BRAF melanoma cells to RAF inhibitors in vitro and in vivo, while CARF knockdown reversed the enhanced sensitivity. In summary, these findings suggest that SAMMSON may function as a new mediator of adaptive resistance to RAF inhibitors in melanoma by modulating CARF-p53 signaling. Significance: This study highlights the role of a SAMMSON/CARF/p53 signaling axis in modulating the adaptive resistance of mutant BRAF melanoma to RAF inhibitors.

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GB/T 7714 Han, Shujun , Yan, Yuwei , Ren, Yibo et al. LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells [J]. | CANCER RESEARCH , 2021 , 81 (11) : 2918-2929 .
MLA Han, Shujun et al. "LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells" . | CANCER RESEARCH 81 . 11 (2021) : 2918-2929 .
APA Han, Shujun , Yan, Yuwei , Ren, Yibo , Hu, Yiming , Wang, Yan , Chen, Lei et al. LncRNA SAMMSON Mediates Adaptive Resistance to RAF Inhibition in BRAF-Mutant Melanoma Cells . | CANCER RESEARCH , 2021 , 81 (11) , 2918-2929 .
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Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status SCIE PubMed
期刊论文 | 2021 , 10 (11) | ANTIOXIDANTS
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NF-E2-related factor 2 (Nrf2), the key transcription regulator of phase II enzymes, has been considered beneficial for neuronal protection. We previously designed a novel chalcone analog, 1-(2,3,4-trimethoxyphenyl)-2-(3,4,5-trimethoxyphenyl)-acrylketone (Tak), that could specifically activate Nrf2 in vitro. Here, we report that Tak confers significant hippocampal neuronal protection both in vitro and in vivo. Treatment with Tak has no significant toxicity on cultured neuronal cells. Instead, Tak increases cellular ATP production by increasing mitochondrial function and decreases the levels of reactive oxygen species by activating Nrf2-mediated phase II enzyme expression. Tak pretreatment prevents glutamate-induced excitotoxic neuronal death accompanied by suppressed mitochondrial respiration, increased superoxide production, and activation of apoptosis. Further investigation indicates that the protective effect of Tak is mediated by the Akt signaling pathway. Meanwhile, Tak administration in mice can sufficiently abrogate scopolamine-induced cognitive impairment via decreasing hippocampal oxidative stress. In addition, consistent benefits are also observed in an energy stress mouse model under a high-fat diet, as the administration of Tak remarkably increases Akt signaling-mediated antioxidative enzyme expression and prevents hippocampal neuronal apoptosis without significant effect on the mouse metabolic status. Overall, our study demonstrates that Tak protects cognitive function by Akt-mediated Nrf2 activation to maintain redox status both vivo and in vitro, suggesting that Tak is a promising pharmacological candidate for the treatment of oxidative neuronal diseases.

Keyword :

Akt hippocampus mitochondrial function Nrf2 phase II enzymes

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GB/T 7714 Cui, Yuting , Xiong, Yue , Li, Hua et al. Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status [J]. | ANTIOXIDANTS , 2021 , 10 (11) .
MLA Cui, Yuting et al. "Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status" . | ANTIOXIDANTS 10 . 11 (2021) .
APA Cui, Yuting , Xiong, Yue , Li, Hua , Zeng, Mengqi , Wang, Yan , Li, Yuan et al. Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status . | ANTIOXIDANTS , 2021 , 10 (11) .
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Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice SCIE PubMed
期刊论文 | 2021 , 10 (11) | CELLS
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High-density lipoprotein (HDL) cholesterol levels are closely associated with human health and diseases. To identify genes modulating plasma HDL levels, we integrated HDL measurements and multi-omics data collected from diverse mouse cohorts and combined a list of systems genetics methods, including quantitative trait loci (QTL) mapping analysis, mediation analysis, transcriptome-wide association analysis (TWAS), and correlation analysis. We confirmed a significant and conserved QTL for plasma HDL on chromosome 1 and identified that Tstd1 liver transcript correlates with plasma HDL in several independent mouse cohorts, suggesting Tstd1 may be a potential modulator of plasma HDL levels. Correlation analysis using over 70 transcriptomics datasets in humans and mice revealed consistent correlations between Tstd1 and genes known to be involved in cholesterol and HDL regulation. Consistent with strong enrichment in gene sets related to cholesterol and lipoproteins in the liver, mouse strains with high Tstd1 exhibited higher plasma levels of HDL, total cholesterol and other lipid markers. GeneBridge using large-scale expression datasets identified conserved and positive associations between TSTD1/Tstd1 and mitochondrial pathways, as well as cholesterol and lipid pathways in human, mouse and rat. In summary, we identified Tstd1 as a new modulator of plasma HDL and mitochondrial function through integrative systems analyses, and proposed a new mechanism of HDL modulation and a potential therapeutic target for relevant diseases. This study highlights the value of such integrative approaches in revealing molecular mechanisms of complex traits or diseases.

Keyword :

correlation analysis HDL integrative analysis mediation analysis mitochondria quantitative trait loci (QTL) systems genetics transcriptome-wide association analysis (TWAS)

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GB/T 7714 Zheng, Adi , Li, Hao , Feng, Zhihui et al. Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice [J]. | CELLS , 2021 , 10 (11) .
MLA Zheng, Adi et al. "Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice" . | CELLS 10 . 11 (2021) .
APA Zheng, Adi , Li, Hao , Feng, Zhihui , Liu, Jiankang . Integrative Analyses Reveal Tstd1 as a Potential Modulator of HDL Cholesterol and Mitochondrial Function in Mice . | CELLS , 2021 , 10 (11) .
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Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance EI SCIE PubMed
期刊论文 | 2021 , 8 (11) | ADVANCED SCIENCE
WoS CC Cited Count: 7
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Mitochondrial epigenetics is rising as intriguing notion for its potential involvement in aging and diseases, while the details remain largely unexplored. Here it is shown that among the 13 mitochondrial DNA (mtDNA) encoded genes, NADH-dehydrogenase 6 (ND6) transcript is primarily decreased in obese and type 2 diabetes populations, which negatively correlates with its distinctive hypermethylation. Hepatic mtDNA sequencing in mice unveils that ND6 presents the highest methylation level, which dramatically increases under diabetic condition due to enhanced mitochondrial translocation of DNA methyltransferase 1 (DNMT1) promoted by free fatty acid through adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) activation. Hepatic knockdown of ND6 or overexpression of Dnmt1 similarly impairs mitochondrial function and induces systemic insulin resistance both in vivo and in vitro. Genetic or chemical targeting hepatic DNMT1 shows significant benefits against insulin resistance associated metabolic disorders. These findings highlight the pivotal role of ND6 epigenetic network in regulating mitochondrial function and onset of insulin resistance, shedding light on potential preventive and therapeutic strategies of insulin resistance and related metabolic disorders from a perspective of mitochondrial epigenetics.

Keyword :

dehydrogenase 6 (ND6) DNA methyltransferase 1 (DNMT1) insulin resistance mitochondrial dysfunction mitochondrial NADH&#8208 obesity and type 2 diabetes mellitus (T2DM)

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GB/T 7714 Cao, Ke , Lv, Weiqiang , Wang, Xueqiang et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance [J]. | ADVANCED SCIENCE , 2021 , 8 (11) .
MLA Cao, Ke et al. "Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance" . | ADVANCED SCIENCE 8 . 11 (2021) .
APA Cao, Ke , Lv, Weiqiang , Wang, Xueqiang , Dong, Shanshan , Liu, Xuyun , Yang, Tielin et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance . | ADVANCED SCIENCE , 2021 , 8 (11) .
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