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  1. Article ; Online: Mitochondrial Dysfunction in Cardiovascular Diseases

    Jiaqi Yang / Qianyun Guo / Xunxun Feng / Yang Liu / Yujie Zhou

    Frontiers in Cell and Developmental Biology, Vol

    Potential Targets for Treatment

    2022  Volume 10

    Abstract: Cardiovascular diseases (CVDs) are serious public health issues and are responsible for nearly one-third of global deaths. Mitochondrial dysfunction is accountable for the development of most CVDs. Mitochondria produce adenosine triphosphate through ... ...

    Abstract Cardiovascular diseases (CVDs) are serious public health issues and are responsible for nearly one-third of global deaths. Mitochondrial dysfunction is accountable for the development of most CVDs. Mitochondria produce adenosine triphosphate through oxidative phosphorylation and inevitably generate reactive oxygen species (ROS). Excessive ROS causes mitochondrial dysfunction and cell death. Mitochondria can protect against these damages via the regulation of mitochondrial homeostasis. In recent years, mitochondria-targeted therapy for CVDs has attracted increasing attention. Various studies have confirmed that clinical drugs (β-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor-II blockers) against CVDs have mitochondrial protective functions. An increasing number of cardiac mitochondrial targets have shown their cardioprotective effects in experimental and clinical studies. Here, we briefly introduce the mechanisms of mitochondrial dysfunction and summarize the progression of mitochondrial targets against CVDs, which may provide ideas for experimental studies and clinical trials.
    Keywords cardiovascular diseases ; mitochondrial dysfunction ; reactive oxygen species ; mitophagy ; mitochondrial therapy ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Anion Gap Was Associated with Inhospital Mortality and Adverse Clinical Outcomes of Coronary Care Unit Patients

    Tienan Sun / Chenghui Cai / Hua Shen / Jiaqi Yang / Qianyun Guo / Jingrui Zhang / Biyang Zhang / Yaodong Ding / Yujie Zhou

    BioMed Research International, Vol

    2020  Volume 2020

    Abstract: Background. Anion gap (AG) has been proved to be associated with prognosis of many cardiovascular diseases. This study is aimed at exploring the association of AG with inhospital all-cause mortality and adverse clinical outcomes in coronary care unit ( ... ...

    Abstract Background. Anion gap (AG) has been proved to be associated with prognosis of many cardiovascular diseases. This study is aimed at exploring the association of AG with inhospital all-cause mortality and adverse clinical outcomes in coronary care unit (CCU) patients. Method. All data of this study was extracted from Medical Information Mart for Intensive Care III (MIMIC-III, version 1.4) database. All patients were divided into four groups according to AG quartiles. Primary outcome was inhospital all-cause mortality. Lowess smoothing curve was drawn to describe the overall trend of inhospital mortality. Binary logistic regression analysis was performed to determine the independent effect of AG on inhospital mortality. Result. A total of 3593 patients were enrolled in this study. In unadjusted model, as AG quartiles increased, inhospital mortality increased significantly, OR increased stepwise from quartile 2 (OR, 95% CI: 1.01, 0.74-1.38, P=0.958) to quartile 4 (OR, 95% CI: 2.72, 2.08-3.55, P<0.001). After adjusting for possible confounding variables, this association was attenuated, but still remained statistically significant (quartile 1 vs. quartile 4: OR, 95% CI: 1.02, 0.72-1.45 vs. 1.49, 1.07-2.09, P=0.019). Moreover, CCU mortality (P<0.001) and rate of acute kidney injury (P<0.001) were proved to be higher in the highest AG quartiles. Length of CCU (P<0.001) and hospital stay (P<0.001) prolonged significantly in higher AG quartiles. Maximum sequential organ failure assessment score (SOFA) (P<0.001) and simplified acute physiology score II (SAPSII) (P<0.001) increased significantly as AG quartiles increased. Moderate predictive ability of AG on inhospital (AUC: 0.6291), CCU mortality (AUC: 0.6355), and acute kidney injury (AUC: 0.6096) was confirmed. The interactions were proved to be significant in hypercholesterolemia, congestive heart failure, chronic lung disease, respiratory failure, oral anticoagulants, Beta-blocks, angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), and vasopressin treatment subgroups. Conclusion. AG was an independent risk factor of inhospital all-cause mortality and was associated with adverse clinical outcomes in CCU patients.
    Keywords Medicine ; R
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Association between Neutrophil Percentage-to-Albumin Ratio and All-Cause Mortality in Critically Ill Patients with Coronary Artery Disease

    Tienan Sun / Hua Shen / Qianyun Guo / Jiaqi Yang / Guangyao Zhai / Jingrui Zhang / Biyang Zhang / Yaodong Ding / Chenghui Cai / Yujie Zhou

    BioMed Research International, Vol

    2020  Volume 2020

    Abstract: Background. Neutrophil percentage-to-albumin ratio (NPAR) has been proved to be associated with clinical outcome of many diseases. This study was aimed at exploring the independent effect of NPAR on all-cause mortality of critically ill patients with ... ...

    Abstract Background. Neutrophil percentage-to-albumin ratio (NPAR) has been proved to be associated with clinical outcome of many diseases. This study was aimed at exploring the independent effect of NPAR on all-cause mortality of critically ill patients with coronary artery disease (CAD). Method. NPAR was calculated as neutrophil percentage numerator divided by serum albumin concentration. Clinical endpoints were 30-day, 90-day, and 365-day all-cause mortality. Multivariable Cox proportional hazard models were performed to confirm the association between NPAR and all-cause mortality. Result. 3106 patients with CAD were enrolled. All-cause mortality rates of 30 days (P<0.001), 90 days (P<0.001), and 365 days (P<0.001) increased as NPAR tertiles increased. And after adjusting for possible confounding variables, NPAR was still independently associated with 30-day (third tertile group versus first tertile group: HR, 95% CI: 1.924, 1.471-2.516; P for trend < 0.001), 90-day (third tertile group versus first tertile group: HR, 95% CI: 2.053, 1.646-2.560; P for trend < 0.001), and 365-day (third tertile group versus first tertile group: HR, 95% CI: 2.063, 1.717-2.480; P for trend < 0.001) all-cause mortality in patients with CAD. Subgroup analysis did not find obvious interaction in most subgroups. Conclusion. NPAR was independently correlated with 30-day, 60-day, and 365-day all-cause mortality in critically ill patients with CAD.
    Keywords Medicine ; R
    Subject code 610
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Metformin and Resveratrol Inhibited High Glucose-Induced Metabolic Memory of Endothelial Senescence through SIRT1/p300/p53/p21 Pathway.

    Erli Zhang / Qianyun Guo / Haiyang Gao / Ruixia Xu / Siyong Teng / Yongjian Wu

    PLoS ONE, Vol 10, Iss 12, p e

    2015  Volume 0143814

    Abstract: Endothelial senescence plays crucial roles in diabetic vascular complication. Recent evidence indicated that transient hyperglycaemia could potentiate persistent diabetic vascular complications, a phenomenon known as "metabolic memory." Although SIRT1 ... ...

    Abstract Endothelial senescence plays crucial roles in diabetic vascular complication. Recent evidence indicated that transient hyperglycaemia could potentiate persistent diabetic vascular complications, a phenomenon known as "metabolic memory." Although SIRT1 has been demonstrated to mediate high glucose-induced endothelial senescence, whether and how "metabolic memory" would affect endothelial senescence through SIRT1 signaling remains largely unknown. In this study, we investigated the involvement of SIRT1 axis as well as the protective effects of resveratrol (RSV) and metformin (MET), two potent SIRT1 activators, during the occurrence of "metabolic memory" of cellular senescence (senescent "memory"). Human umbilical vascular endothelial cells (HUVECs) were cultured in either normal glucose (NG)/high glucose (HG) media for 6 days, or 3 days of HG followed by 3 days of NG (HN), with or without RSV or MET treatment. It was shown that HN incubation triggered persistent downregulation of deacetylase SIRT1 and upregulation of acetyltransferase p300, leading to sustained hyperacetylation (at K382) and activation of p53, and subsequent p53/p21-mediated senescent "memory." In contrast, senescent "memory" was abrogated by overexpression of SIRT1 or knockdown of p300. Interestingly, we found that SIRT1 and p300 could regulate each other in response to HN stimulation, suggesting that a delicate balance between acetyltransferases and deacetylases may be particularly important for sustained acetylation and activation of non-histone proteins (such as p53), and eventually the occurrence of "metabolic memory." Furthermore, we found that RSV or MET treatment prevented senescent "memory" by modulating SIRT1/p300/p53/p21 pathway. Notably, early and continuous treatment of MET, but not RSV, was particularly important for preventing senescent "memory." In conclusion, short-term high glucose stimulation could induce sustained endothelial senescence via SIRT1/p300/p53/p21 pathway. RVS or MET treatment could enhance SIRT1-mediated signaling ...
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Non-coding cancer driver candidates identified with a sample- and position-specific model of the somatic mutation rate

    Malene Juul / Johanna Bertl / Qianyun Guo / Morten Muhlig Nielsen / Michał Świtnicki / Henrik Hornshøj / Tobias Madsen / Asger Hobolth / Jakob Skou Pedersen

    eLife, Vol

    2017  Volume 6

    Abstract: Non-coding mutations may drive cancer development. Statistical detection of non-coding driver regions is challenged by a varying mutation rate and uncertainty of functional impact. Here, we develop a statistically founded non-coding driver-detection ... ...

    Abstract Non-coding mutations may drive cancer development. Statistical detection of non-coding driver regions is challenged by a varying mutation rate and uncertainty of functional impact. Here, we develop a statistically founded non-coding driver-detection method, ncdDetect, which includes sample-specific mutational signatures, long-range mutation rate variation, and position-specific impact measures. Using ncdDetect, we screened non-coding regulatory regions of protein-coding genes across a pan-cancer set of whole-genomes (n = 505), which top-ranked known drivers and identified new candidates. For individual candidates, presence of non-coding mutations associates with altered expression or decreased patient survival across an independent pan-cancer sample set (n = 5454). This includes an antigen-presenting gene (CD1A), where 5’UTR mutations correlate significantly with decreased survival in melanoma. Additionally, mutations in a base-excision-repair gene (SMUG1) correlate with a C-to-T mutational-signature. Overall, we find that a rich model of mutational heterogeneity facilitates non-coding driver identification and integrative analysis points to candidates of potential clinical relevance.
    Keywords cancer ; driver detection ; non-coding mutations ; mutational processes ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-03-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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