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  1. Article ; Online: Response by Zhang and Wang to Letter Regarding Article, "Integrated Stress Response Couples Mitochondrial Protein Translation With Oxidative Stress Control".

    Zhang, Guangyu / Wang, Zhao V

    Circulation

    2022  Volume 145, Issue 14, Page(s) e804–e805

    Language English
    Publishing date 2022-04-04
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.122.059422
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: NAD in pathological cardiac remodeling: Metabolic regulation and beyond.

    Norambuena-Soto, Ignacio / Deng, Yingfeng / Brenner, Charles / Lavandero, Sergio / Wang, Zhao V

    Biochimica et biophysica acta. Molecular basis of disease

    2024  Volume 1870, Issue 3, Page(s) 167038

    Abstract: Nicotinamide adenine dinucleotide (NAD) coenzymes are carriers of high energy electrons in metabolism and also play critical roles in numerous signaling pathways. NAD metabolism is decreased in various cardiovascular diseases. Importantly, stimulation of ...

    Abstract Nicotinamide adenine dinucleotide (NAD) coenzymes are carriers of high energy electrons in metabolism and also play critical roles in numerous signaling pathways. NAD metabolism is decreased in various cardiovascular diseases. Importantly, stimulation of NAD biosynthesis protects against heart disease under different pathological conditions. In this review, we describe pathways for both generation and catabolism of NAD coenzymes and the respective changes of these pathways in the heart under cardiac diseases, including pressure overload, myocardial infarction, cardiometabolic disease, cancer treatment cardiotoxicity, and heart failure. We next provide an update on the strategies and treatments to increase NAD levels, such as supplementation of NAD precursors, in the heart that prevent or reverse cardiomyopathy. We also introduce the approaches to manipulate NAD consumption enzymes to ameliorate cardiac disease. Finally, we discuss the mechanisms associated with improvements in cardiac function by NAD coenzymes, differentiating between mitochondria-dependent effects and those independent of mitochondrial metabolism.
    MeSH term(s) Humans ; NAD/metabolism ; Ventricular Remodeling ; Heart ; Heart Failure ; Coenzymes ; Heart Diseases
    Chemical Substances NAD (0U46U6E8UK) ; Coenzymes
    Language English
    Publishing date 2024-01-27
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2024.167038
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  3. Article ; Online: Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.

    Tran, Diem H / Wang, Zhao V

    Journal of the American Heart Association

    2019  Volume 8, Issue 12, Page(s) e012673

    MeSH term(s) Cardiomegaly/metabolism ; Glucose/metabolism ; Glycolysis ; Heart Failure/metabolism ; Hexosamines/metabolism ; Humans ; Myocardial Ischemia/metabolism ; Pentose Phosphate Pathway ; Polymers/metabolism
    Chemical Substances Hexosamines ; Polymers ; polyol ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2019-06-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.119.012673
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitochondrial Dysfunction in Cardiac Arrhythmias.

    Deng, Jielin / Jiang, Yunqiu / Chen, Zhen Bouman / Rhee, June-Wha / Deng, Yingfeng / Wang, Zhao V

    Cells

    2023  Volume 12, Issue 5

    Abstract: Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. ...

    Abstract Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. In arrhythmias, the homeostatic supply-demand relationship is impaired, which is often accompanied by progressive mitochondrial dysfunction leading to reduced ATP production and elevated reactive oxidative species generation. Furthermore, ion homeostasis, membrane excitability, and cardiac structure can be disrupted through pathological changes in gap junctions and inflammatory signaling, which results in impaired cardiac electrical homeostasis. Herein, we review the electrical and molecular mechanisms of cardiac arrhythmias, with a particular focus on mitochondrial dysfunction in ionic regulation and gap junction action. We provide an update on inherited and acquired mitochondrial dysfunction to explore the pathophysiology of different types of arrhythmias. In addition, we highlight the role of mitochondria in bradyarrhythmia, including sinus node dysfunction and atrioventricular node dysfunction. Finally, we discuss how confounding factors, such as aging, gut microbiome, cardiac reperfusion injury, and electrical stimulation, modulate mitochondrial function and cause tachyarrhythmia.
    MeSH term(s) Humans ; Reactive Oxygen Species ; Arrhythmias, Cardiac/pathology ; Heart ; Mitochondria/pathology ; Adenosine Triphosphate
    Chemical Substances Reactive Oxygen Species ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-02-21
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12050679
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  5. Article ; Online: Diverging consequences of hexosamine biosynthesis in cardiovascular disease.

    Li, Qinfeng / Taegtmeyer, Heinrich / Wang, Zhao V

    Journal of molecular and cellular cardiology

    2020  Volume 153, Page(s) 104–105

    MeSH term(s) Animals ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Hexosamines/biosynthesis ; Humans ; Muscle Proteins/chemistry ; Muscle Proteins/metabolism ; Protein Processing, Post-Translational
    Chemical Substances Hexosamines ; Muscle Proteins
    Language English
    Publishing date 2020-12-30
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2020.12.016
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 426: Show issues Location:
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  6. Article: Simultaneous proteome localization and turnover analysis reveals spatiotemporal features of protein homeostasis disruptions.

    Currie, Jordan / Manda, Vyshnavi / Robinson, Sean K / Lai, Celine / Agnihotri, Vertica / Hidalgo, Veronica / Ludwig, R W / Zhang, Kai / Pavelka, Jay / Wang, Zhao V / Rhee, June-Wha / Lam, Maggie P Y / Lau, Edward

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The functions of proteins depend on their spatial and temporal distributions, which are not directly measured by static protein abundance. Under endoplasmic reticulum (ER) stress, the unfolded protein response (UPR) pathway remediates proteostasis in ... ...

    Abstract The functions of proteins depend on their spatial and temporal distributions, which are not directly measured by static protein abundance. Under endoplasmic reticulum (ER) stress, the unfolded protein response (UPR) pathway remediates proteostasis in part by altering the turnover kinetics and spatial distribution of proteins. A global view of these spatiotemporal changes has yet to emerge and it is unknown how they affect different cellular compartments and pathways. Here we describe a mass spectrometry-based proteomics strategy and data analysis pipeline, termed Simultaneous Proteome Localization and Turnover (SPLAT), to measure concurrently the changes in protein turnover and subcellular distribution in the same experiment. Investigating two common UPR models of thapsigargin and tunicamycin challenge in human AC16 cells, we find that the changes in protein turnover kinetics during UPR varies across subcellular localizations, with overall slowdown but an acceleration in endoplasmic reticulum and Golgi proteins involved in stress response. In parallel, the spatial proteomics component of the experiment revealed an externalization of amino acid transporters and ion channels under UPR, as well as the migration of RNA-binding proteins toward an endosome co-sedimenting compartment. The SPLAT experimental design classifies heavy and light SILAC labeled proteins separately, allowing the observation of differential localization of new and old protein pools and capturing a partition of newly synthesized EGFR and ITGAV to the ER under stress that suggests protein trafficking disruptions. Finally, application of SPLAT toward human induced pluripotent stem cell derived cardiomyocytes (iPSC-CM) exposed to the cancer drug carfilzomib, identified a selective disruption of proteostasis in sarcomeric proteins as a potential mechanism of carfilzomib-mediated cardiotoxicity. Taken together, this study provides a global view into the spatiotemporal dynamics of human cardiac cells and demonstrates a method for inferring the coordinations between spatial and temporal proteome regulations in stress and drug response.
    Language English
    Publishing date 2024-01-17
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.04.521821
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Simultaneous proteome localization and turnover analysis reveals spatiotemporal features of protein homeostasis disruptions.

    Currie, Jordan / Manda, Vyshnavi / Robinson, Sean K / Lai, Celine / Agnihotri, Vertica / Hidalgo, Veronica / Ludwig, R W / Zhang, Kai / Pavelka, Jay / Wang, Zhao V / Rhee, June-Wha / Lam, Maggie P Y / Lau, Edward

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 2207

    Abstract: The spatial and temporal distributions of proteins are critical to protein function, but cannot be directly assessed by measuring protein bundance. Here we describe a mass spectrometry-based proteomics strategy, Simultaneous Proteome Localization and ... ...

    Abstract The spatial and temporal distributions of proteins are critical to protein function, but cannot be directly assessed by measuring protein bundance. Here we describe a mass spectrometry-based proteomics strategy, Simultaneous Proteome Localization and Turnover (SPLAT), to measure concurrently protein turnover rates and subcellular localization in the same experiment. Applying the method, we find that unfolded protein response (UPR) has different effects on protein turnover dependent on their subcellular location in human AC16 cells, with proteome-wide slowdown but acceleration among stress response proteins in the ER and Golgi. In parallel, UPR triggers broad differential localization of proteins including RNA-binding proteins and amino acid transporters. Moreover, we observe newly synthesized proteins including EGFR that show a differential localization under stress than the existing protein pools, reminiscent of protein trafficking disruptions. We next applied SPLAT to an induced pluripotent stem cell derived cardiomyocyte (iPSC-CM) model of cancer drug cardiotoxicity upon treatment with the proteasome inhibitor carfilzomib. Paradoxically, carfilzomib has little effect on global average protein half-life, but may instead selectively disrupt sarcomere protein homeostasis. This study provides a view into the interactions of protein spatial and temporal dynamics and demonstrates a method to examine protein homeostasis regulations in stress and drug response.
    MeSH term(s) Humans ; Proteome/metabolism ; Proteostasis ; Unfolded Protein Response ; Mass Spectrometry ; Golgi Apparatus/metabolism
    Chemical Substances Proteome
    Language English
    Publishing date 2024-03-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-46600-5
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  8. Article ; Online: Adiponectin, the past two decades.

    Wang, Zhao V / Scherer, Philipp E

    Journal of molecular cell biology

    2016  Volume 8, Issue 2, Page(s) 93–100

    Abstract: Adiponectin is an adipocyte-specific factor, first described in 1995. Over the past two decades, numerous studies have elucidated the physiological functions of adiponectin in obesity, diabetes, inflammation, atherosclerosis, and cardiovascular disease. ... ...

    Abstract Adiponectin is an adipocyte-specific factor, first described in 1995. Over the past two decades, numerous studies have elucidated the physiological functions of adiponectin in obesity, diabetes, inflammation, atherosclerosis, and cardiovascular disease. Adiponectin, elicited through cognate receptors, suppresses glucose production in the liver and enhances fatty acid oxidation in skeletal muscle, which together contribute to a beneficial metabolic action in whole body energy homeostasis. Beyond its role in metabolism, adiponectin also protects cells from apoptosis and reduces inflammation in various cell types via receptor-dependent mechanisms. Adiponectin, as a fat-derived hormone, therefore fulfills a critical role as an important messenger to communicate between adipose tissue and other organs. A better understanding of adiponectin actions, including the pros and cons, will advance our insights into basic mechanisms of metabolism and inflammation, and potentially pave the way toward novel means of pharmacological intervention to address pathophysiological changes associated with diabetes, atherosclerosis, and cardiometabolic disease.
    MeSH term(s) Adiponectin/chemistry ; Adiponectin/metabolism ; Animals ; Cells/metabolism ; Humans ; Models, Molecular ; Receptors, Adiponectin/metabolism
    Chemical Substances Adiponectin ; Receptors, Adiponectin
    Language English
    Publishing date 2016-03-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1674-2788
    ISSN (online) 1759-4685
    ISSN 1674-2788
    DOI 10.1093/jmcb/mjw011
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  9. Article ; Online: The integrated stress response in ischemic diseases.

    Zhang, Guangyu / Wang, Xiaoding / Rothermel, Beverly A / Lavandero, Sergio / Wang, Zhao V

    Cell death and differentiation

    2021  Volume 29, Issue 4, Page(s) 750–757

    Abstract: Ischemic disease is among the deadliest and most disabling illnesses. Prominent examples include myocardial infarction and stroke. Most, if not all, underlying pathological changes, including oxidative stress, inflammation, and nutrient deprivation, are ... ...

    Abstract Ischemic disease is among the deadliest and most disabling illnesses. Prominent examples include myocardial infarction and stroke. Most, if not all, underlying pathological changes, including oxidative stress, inflammation, and nutrient deprivation, are potent inducers of the integrated stress response (ISR). Four upstream kinases are involved in ISR signaling that sense a myriad of input stress signals and converge on the phosphorylation of serine 51 of eukaryotic translation initiation factor 2α (eIF2α). As a result, translation initiation is halted, creating a window of opportunity for the cell to repair itself and restore homeostasis. A growing number of studies show strong induction of the ISR in ischemic disease. Genetic and pharmacological evidence suggests that the ISR plays critical roles in disease initiation and progression. Here, we review the basic regulation of the ISR, particularly in response to ischemia, and summarize recent findings relevant to the actions of the ISR in ischemic disease. We then discuss therapeutic opportunities by modulating the ISR to treat ischemic heart disease, brain ischemia, ischemic liver disease, and ischemic kidney disease. Finally, we propose that the ISR represents a promising therapeutic target for alleviating symptoms of ischemic disease and improving clinical outcomes.
    MeSH term(s) Eukaryotic Initiation Factor-2/metabolism ; Homeostasis ; Humans ; Ischemia ; Phosphorylation ; Stress, Physiological
    Chemical Substances Eukaryotic Initiation Factor-2
    Language English
    Publishing date 2021-11-06
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-021-00889-7
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4230: Show issues Location:
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  10. Article ; Online: Diabetic cardiomyopathy: catabolism driving metabolism.

    Wang, Zhao V / Hill, Joseph A

    Circulation

    2015  Volume 131, Issue 9, Page(s) 771–773

    MeSH term(s) Animals ; Carrier Proteins/physiology ; Diabetic Cardiomyopathies/genetics ; Insulin Resistance/genetics ; Lipid Metabolism/genetics ; Male ; PPAR alpha/physiology
    Chemical Substances Carrier Proteins ; MG53 protein, mouse ; PPAR alpha
    Language English
    Publishing date 2015-03-03
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.115.015357
    Database MEDical Literature Analysis and Retrieval System OnLINE

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