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  1. Article ; Online: ApoB SURFs a Ride from the ER to the Golgi.

    Ginsberg, Henry N

    Cell metabolism

    2021  Volume 33, Issue 2, Page(s) 231–233

    Abstract: Chylomicrons and very-low-density lipoproteins (VLDLs) are large, complex cargos that may require specific chaperones for efficient transport from the ER to Golgi. In this issue of Cell Metabolism, Wang et al. (2020) identify SURF4, in coordination with ... ...

    Abstract Chylomicrons and very-low-density lipoproteins (VLDLs) are large, complex cargos that may require specific chaperones for efficient transport from the ER to Golgi. In this issue of Cell Metabolism, Wang et al. (2020) identify SURF4, in coordination with SAR1B, as an essential player in COPII transport of VLDLs from ER to Golgi, suggesting that SURF4 may be a target for approaches aimed at reducing secretion of triglyceride-rich, atherogenic lipoproteins from the liver.
    MeSH term(s) Animals ; Apolipoproteins B/metabolism ; Chylomicrons/metabolism ; Golgi Apparatus/metabolism ; Homeostasis ; Humans ; Lipoproteins/metabolism ; Membrane Proteins ; Mice ; Monomeric GTP-Binding Proteins
    Chemical Substances Apolipoproteins B ; Chylomicrons ; Lipoproteins ; Membrane Proteins ; SURF4 protein, human ; Surf4 protein, mouse ; SAR1B protein, human (EC 3.6.1.-) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2021-02-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2021.01.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Basic and translational evidence supporting the role of TM6SF2 in VLDL metabolism.

    Liu, Jing / Ginsberg, Henry N / Reyes-Soffer, Gissette

    Current opinion in lipidology

    2024  Volume 35, Issue 3, Page(s) 157–161

    Abstract: Purpose of review: Transmembrane 6 superfamily member 2 ( TM6SF2 ) gene was identified through exome-wide studies in 2014. A genetic variant from glutamic acid to lysine substitution at amino acid position 167 (NM_001001524.3:c.499G> A) (p.Gln167Lys/p ... ...

    Abstract Purpose of review: Transmembrane 6 superfamily member 2 ( TM6SF2 ) gene was identified through exome-wide studies in 2014. A genetic variant from glutamic acid to lysine substitution at amino acid position 167 (NM_001001524.3:c.499G> A) (p.Gln167Lys/p.E167K, rs58542926) was discovered (p.E167K) to be highly associated with increased hepatic fat content and reduced levels of plasma triglycerides and LDL cholesterol. In this review, we focus on the discovery of TM6SF2 and its role in VLDL secretion pathways. Human data suggest TM6SF2 is linked to hepatic steatosis and cardiovascular disease (CVD), hence understanding its metabolic pathways is of high scientific interest.
    Recent findings: Since its discovery, completed research studies in cell, rodent and human models have defined the role of TM6SF2 and its links to human disease. TM6SF2 resides in the endoplasmic reticulum (ER) and the ER-Golgi interface and helps with the lipidation of nascent VLDL, the main carrier of triglycerides from the liver to the periphery. Consistent results from cells and rodents indicated that the secretion of triglycerides is reduced in carriers of the p.E167K variant or when hepatic TM6SF2 is deleted. However, data for secretion of APOB, the main protein of VLDL particles responsible for triglycerides transport, are inconsistent.
    Summary: The identification of genetic variants that are highly associated with human disease presentation should be followed by the validation and investigation into the pathways that regulate disease mechanisms. In this review, we highlight the role of TM6SF2 and its role in processing of liver triglycerides.
    MeSH term(s) Humans ; Animals ; Membrane Proteins/metabolism ; Membrane Proteins/genetics ; Lipoproteins, VLDL/metabolism ; Translational Research, Biomedical
    Chemical Substances Membrane Proteins ; TM6SF2 protein, human ; Lipoproteins, VLDL
    Language English
    Publishing date 2024-03-08
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1045394-5
    ISSN 1473-6535 ; 0957-9672
    ISSN (online) 1473-6535
    ISSN 0957-9672
    DOI 10.1097/MOL.0000000000000930
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Complex regulation of fatty liver disease.

    Ginsberg, Henry N / Mani, Arya

    Science (New York, N.Y.)

    2022  Volume 376, Issue 6590, Page(s) 247–248

    Abstract: Hepatic lipogenesis is fine-tuned by mechanistic target of rapamycin (mTOR) signaling. ...

    Abstract Hepatic lipogenesis is fine-tuned by mechanistic target of rapamycin (mTOR) signaling.
    MeSH term(s) Humans ; Lipogenesis ; Liver/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Signal Transduction
    Chemical Substances Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2022-04-14
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abp8276
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  4. Article ; Online: Selective Trafficking of Fatty Acids in the Liver: Add Them2 to the List of Influencers.

    Ginsberg, Henry N

    Hepatology (Baltimore, Md.)

    2019  Volume 70, Issue 2, Page(s) 462–464

    MeSH term(s) Fatty Acids ; Lipogenesis ; Liver ; Triglycerides
    Chemical Substances Fatty Acids ; Triglycerides
    Language English
    Publishing date 2019-07-15
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30800
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  5. Article ; Online: Broadening the Scope of Dyslipidemia Therapy by Targeting APOC3 (Apolipoprotein C3) and ANGPTL3 (Angiopoietin-Like Protein 3).

    Ginsberg, Henry N / Goldberg, Ira J

    Arteriosclerosis, thrombosis, and vascular biology

    2022  Volume 43, Issue 3, Page(s) 388–398

    Abstract: The positive relationship between increased levels of circulating triglycerides and cardiovascular events has been observed for decades. Driven by genetic cohort studies, inhibitors of APOC3 (apolipoprotein C3) and ANGPTL (angiopoietin-like protein) 3 ... ...

    Abstract The positive relationship between increased levels of circulating triglycerides and cardiovascular events has been observed for decades. Driven by genetic cohort studies, inhibitors of APOC3 (apolipoprotein C3) and ANGPTL (angiopoietin-like protein) 3 that reduce circulating triglycerides are poised to enter clinical practice. We will review the biology of how inhibition of these 2 proteins affects circulating lipoproteins as well as the current state of clinical development of monoclonal antibodies, antisense oligonucleotides, and silencing RNAs targeting APOC3 and ANGPTL3.
    MeSH term(s) Humans ; Angiopoietin-Like Protein 3 ; Angiopoietin-like Proteins/genetics ; Apolipoprotein C-III ; Triglycerides/metabolism ; Dyslipidemias/drug therapy
    Chemical Substances Angiopoietin-Like Protein 3 ; Angiopoietin-like Proteins ; Apolipoprotein C-III ; Triglycerides ; ANGPTL3 protein, human
    Language English
    Publishing date 2022-12-29
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.122.317966
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1705: Show issues Location:
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  6. Article ; Online: New, Novel Lipid-Lowering Agents for Reducing Cardiovascular Risk: Beyond Statins.

    Kim, Kyuho / Ginsberg, Henry N / Choi, Sung Hee

    Diabetes & metabolism journal

    2022  Volume 46, Issue 5, Page(s) 817–818

    Language English
    Publishing date 2022-09-19
    Publishing country Korea (South)
    Document type Journal Article ; Published Erratum
    ZDB-ID 2602402-0
    ISSN 2233-6087 ; 2233-6087
    ISSN (online) 2233-6087
    ISSN 2233-6087
    DOI 10.4093/dmj.2022.0295
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  7. Article ; Online: VLDL Biogenesis and Secretion: It Takes a Village.

    van Zwol, Willemien / van de Sluis, Bart / Ginsberg, Henry N / Kuivenhoven, Jan Albert

    Circulation research

    2024  Volume 134, Issue 2, Page(s) 226–244

    Abstract: The production and secretion of VLDLs (very-low-density lipoproteins) by hepatocytes has a direct impact on liver fat content, as well as the concentrations of cholesterol and triglycerides in the circulation and thus affects both liver and ... ...

    Abstract The production and secretion of VLDLs (very-low-density lipoproteins) by hepatocytes has a direct impact on liver fat content, as well as the concentrations of cholesterol and triglycerides in the circulation and thus affects both liver and cardiovascular health, respectively. Importantly, insulin resistance, excess caloric intake, and lack of physical activity are associated with overproduction of VLDL, hepatic steatosis, and increased plasma levels of atherogenic lipoproteins. Cholesterol and triglycerides in remnant particles generated by VLDL lipolysis are risk factors for atherosclerotic cardiovascular disease and have garnered increasing attention over the last few decades. Presently, however, increased risk of atherosclerosis is not the only concern when considering today's cardiometabolic patients, as they often also experience hepatic steatosis, a prevalent disorder that can progress to steatohepatitis and cirrhosis. This duality of metabolic risk highlights the importance of understanding the molecular regulation of the biogenesis of VLDL, the lipoprotein that transports triglycerides and cholesterol out of the liver. Fortunately, there has been a resurgence of interest in the intracellular assembly, trafficking, degradation, and secretion of VLDL by hepatocytes, which has led to many exciting new molecular insights that are the topic of this review. Increasing our understanding of the biology of this pathway will aid to the identification of novel therapeutic targets to improve both the cardiovascular and the hepatic health of cardiometabolic patients. This review focuses, for the first time, on this duality.
    MeSH term(s) Humans ; Lipoproteins ; Lipoproteins, VLDL ; Triglycerides ; Liver/metabolism ; Cholesterol/metabolism ; Fatty Liver/metabolism ; Cardiovascular Diseases/metabolism
    Chemical Substances Lipoproteins ; Lipoproteins, VLDL ; Triglycerides ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2024-01-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323284
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    Ui IV Zs.70: Show issues Location:
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  8. Article ; Online: New, Novel Lipid-Lowering Agents for Reducing Cardiovascular Risk: Beyond Statins.

    Kim, Kyuho / Ginsberg, Henry N / Choi, Sung Hee

    Diabetes & metabolism journal

    2022  Volume 46, Issue 4, Page(s) 517–532

    Abstract: Statins are the cornerstone of the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD). However, even under optimal statin therapy, a significant residual ASCVD risk remains. Therefore, there has been an unmet clinical need for ... ...

    Abstract Statins are the cornerstone of the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD). However, even under optimal statin therapy, a significant residual ASCVD risk remains. Therefore, there has been an unmet clinical need for novel lipid-lowering agents that can target low-density lipoprotein cholesterol (LDL-C) and other atherogenic particles. During the past decade, several drugs have been developed for the treatment of dyslipidemia. Inclisiran, a small interfering RNA that targets proprotein convertase subtilisin/kexin type 9 (PCSK9), shows comparable effects to that of PCSK9 monoclonal antibodies. Bempedoic acid, an ATP citrate lyase inhibitor, is a valuable treatment option for the patients with statin intolerance. Pemafibrate, the first selective peroxisome proliferator-activated receptor alpha modulator, showed a favorable benefit-risk balance in phase 2 trial, but the large clinical phase 3 trial (PROMINENT) was recently stopped for futility based on a late interim analysis. High dose icosapent ethyl, a modified eicosapentaenoic acid preparation, shows cardiovascular benefits. Evinacumab, an angiopoietin-like 3 (ANGPTL3) monoclonal antibody, reduces plasma LDL-C levels in patients with refractory hypercholesterolemia. Novel antisense oligonucleotides targeting apolipoprotein C3 (apoC3), ANGPTL3, and lipoprotein(a) have significantly attenuated the levels of their target molecules with beneficial effects on associated dyslipidemias. Apolipoprotein A1 (apoA1) is considered as a potential treatment to exploit the athero-protective effects of high-density lipoprotein cholesterol (HDL-C), but solid clinical evidence is necessary. In this review, we discuss the mode of action and clinical outcomes of these novel lipid-lowering agents beyond statins.
    MeSH term(s) Angiopoietin-Like Protein 3 ; Angiopoietin-like Proteins ; Atherosclerosis/drug therapy ; Atherosclerosis/prevention & control ; Cardiovascular Diseases/complications ; Cholesterol, LDL ; Dyslipidemias/complications ; Dyslipidemias/drug therapy ; Heart Disease Risk Factors ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Hypolipidemic Agents/therapeutic use ; Proprotein Convertase 9/therapeutic use ; Risk Factors
    Chemical Substances ANGPTL3 protein, human ; Angiopoietin-Like Protein 3 ; Angiopoietin-like Proteins ; Cholesterol, LDL ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hypolipidemic Agents ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-)
    Language English
    Publishing date 2022-07-27
    Publishing country Korea (South)
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2602402-0
    ISSN 2233-6087 ; 2233-6087
    ISSN (online) 2233-6087
    ISSN 2233-6087
    DOI 10.4093/dmj.2022.0198
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Book ; Conference proceedings: A Symposium Implications of Insulin Resistance - Concerns Beyond Glucose

    Ginsberg, Henry N.

    based on a CME symposium held in August 1998 in Colorado Springs, Colorado

    (The American journal of cardiology ; 84,1A)

    1999  

    Title variant Implications of insulin resistance - concerns beyond glucose
    Event/congress Symposium Implications of Insulin Resistance - Concerns Beyond Glucose (1998, ColoradoSpringsColo.)
    Author's details guest ed.: Henry N. Ginsberg
    Series title The American journal of cardiology ; 84,1A
    Collection
    Language English
    Size 48J S. : Ill., graph. Darst.
    Publisher Excerpta Medica
    Publishing place New York, NY
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT010747567
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Ui IV Zs 73 -84,1A- verfügbar in Königswinter Königswinter

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  10. Article ; Online: Evolocumab Treatment of Hypercholesterolemia in OSLER-1: Enduring Efficacy, Tolerability, and Safety Over 5 Years.

    Chapman, M John / Ginsberg, Henry N

    Journal of the American College of Cardiology

    2019  Volume 74, Issue 17, Page(s) 2147–2149

    MeSH term(s) Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Humans ; Hypercholesterolemia ; Proprotein Convertase 9
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Proprotein Convertase 9 (EC 3.4.21.-) ; evolocumab (LKC0U3A8NJ)
    Language English
    Publishing date 2019-01-01
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2019.07.087
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