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  1. Book ; Online ; E-Book: Biochemistry of apoptosis and autophagy

    Kirshenbaum, Lorrie A.

    (Advances in biochemistry in health and disease ; 18)

    2022  

    Author's details Lorrie A. Kirshenbaum editor
    Series title Advances in biochemistry in health and disease ; 18
    Collection
    Keywords Electronic books
    Language English
    Size 1 Online-Ressource (xvi, 283 Seiten), Illustrationen, Diagramme
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021202510
    ISBN 978-3-030-78799-8 ; 9783030787981 ; 3-030-78799-0 ; 3030787982
    DOI 10.1007/978-3-030-78799-8
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Biochemistry of hypertrophy and heart failure

    Kirshenbaum, Lorrie A.

    (Developments in molecular and cellular biochemistry ; 43)

    2003  

    Author's details ed. by Lorrie A. Kirshenbaum
    Series title Developments in molecular and cellular biochemistry ; 43
    Collection
    Keywords Chronische Herzinsuffizienz ; Herzhypertrophie ; Pathobiochemie
    Subject Pathologische Biochemie ; Kardiale Hypertrophie
    Language English
    Size 163 S. : zahlr. graph. Darst.
    Publisher Kluwer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    Note Aus:: Molecular and cellular biochemistry ; 251.2003,1/2
    HBZ-ID HT013841223
    ISBN 1-4020-7434-4 ; 978-1-4020-7434-9
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: Unc51-like-kinase 1-mediated mitophagy prevents pathological cardiac remodelling and heart failure.

    Dhingra, Rimpy / Kirshenbaum, Lorrie A

    Cardiovascular research

    2022  Volume 118, Issue 12, Page(s) 2561–2563

    MeSH term(s) Autophagy-Related Protein-1 Homolog ; Heart ; Heart Failure ; Humans ; Intracellular Signaling Peptides and Proteins ; Mitophagy ; Ventricular Remodeling
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; ULK1 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2022-07-02
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvac101
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: DIAPH1-MFN2 interaction decreases the endoplasmic reticulum-mitochondrial distance and promotes cardiac injury following myocardial ischemia.

    Kirshenbaum, Lorrie A / Dhingra, Rimpy / Bravo-Sagua, Roberto / Lavandero, Sergio

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1469

    MeSH term(s) Humans ; Myocardial Ischemia ; Endoplasmic Reticulum ; Coronary Artery Disease ; Endoplasmic Reticulum Stress ; Apoptosis ; Myocytes, Cardiac ; Formins ; GTP Phosphohydrolases ; Mitochondrial Proteins
    Chemical Substances DIAPH1 protein, human ; Formins ; MFN2 protein, human (EC 3.6.1.-) ; GTP Phosphohydrolases (EC 3.6.1.-) ; Mitochondrial Proteins
    Language English
    Publishing date 2024-02-17
    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/s41467-024-45560-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Circadian-Regulated Cardiac Metabolism Involves Transcription Factor E4BP4.

    Rabinovich-Nikitin, Inna / Kirshenbaum, Lorrie A

    JACC. Basic to translational science

    2023  Volume 8, Issue 9, Page(s) 1157–1159

    Language English
    Publishing date 2023-09-25
    Publishing country United States
    Document type Editorial
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2023.06.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: BMAL1 regulates cell cycle progression and angiogenesis of endothelial cells.

    Rabinovich-Nikitin, Inna / Kirshenbaum, Lorrie A

    Cardiovascular research

    2023  Volume 119, Issue 10, Page(s) 1889–1890

    MeSH term(s) ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Endothelial Cells/metabolism ; Cell Cycle ; Morphogenesis
    Chemical Substances ARNTL Transcription Factors
    Language English
    Publishing date 2023-06-29
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Autophagy, Clock Genes, and Cardiovascular Disease.

    Rabinovich-Nikitin, Inna / Kirshenbaum, Eryn / Kirshenbaum, Lorrie A

    The Canadian journal of cardiology

    2023  Volume 39, Issue 12, Page(s) 1772–1780

    Abstract: Circadian rhythms are 24-hour cycles that regulate physical, mental, and behavioural changes of most living organisms. In the heart, circadian rhythms regulate processes such as heart rate, blood pressure, blood coagulability, and vascular tone. However, ...

    Abstract Circadian rhythms are 24-hour cycles that regulate physical, mental, and behavioural changes of most living organisms. In the heart, circadian rhythms regulate processes such as heart rate, blood pressure, blood coagulability, and vascular tone. However, in addition to regulating physiologic processes, circadian rhythms regulate pathophysiologic processes in the heart. In this regard, circadian rhythms regulate the onset, severity, and outcome of many cardiovascular diseases (CVDs), including myocardial infarction, diabetic cardiomyopathy, doxorubicin (Dox)-induced cardiotoxicity, and heart failure. Notably, the underlying mechanism of many of these diseases is linked to impaired cellular quality control processes, such as autophagy. Autophagy is a homeostatic cellular process that regulates the removal of damaged cellular components, allowing their degradation and recycling into their basic constituents for production of cellular energy. Many studies from recent years point to a regulatory link between autophagy and circadian machinery in the control of CVDs. In this review, we highlight the recent discoveries in the field of circadian-induced autophagy in the heart and provide the molecular mechanisms and signalling pathways that underlie the crosstalk between autophagy and clock gene control in response to cardiac injury. Understanding the mechanisms that underlie circadian-induced autophagy in response to cardiac stress may prove to be beneficial in developing novel therapeutic approaches to treat cardiac disease.
    MeSH term(s) Humans ; Cardiovascular Diseases/metabolism ; Circadian Rhythm/genetics ; Autophagy/genetics ; Heart Diseases ; Heart
    Language English
    Publishing date 2023-08-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2023.08.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Response by Dhingra et al to Letter Regarding Article, "Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy".

    Dhingra, Rimpy / Javaheri, Ali / Diwan, Abhinav / Kirshenbaum, Lorrie A

    Circulation

    2023  Volume 147, Issue 13, Page(s) 1051–1052

    MeSH term(s) Humans ; TNF Receptor-Associated Factor 2 ; Cardiomyopathies/chemically induced ; Ubiquitin-Protein Ligases/metabolism ; Mitochondria/metabolism ; Doxorubicin/adverse effects
    Chemical Substances TNF Receptor-Associated Factor 2 ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Doxorubicin (80168379AG)
    Language English
    Publishing date 2023-03-27
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; 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.123.063546
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Intersection of autophagy regulation and circadian rhythms in the heart.

    Rabinovich-Nikitin, Inna / Love, Matthew / Kirshenbaum, Lorrie A

    Biochimica et biophysica acta. Molecular basis of disease

    2022  Volume 1868, Issue 4, Page(s) 166354

    Abstract: Autophagy is a vital cellular mechanism that controls the removal of damaged or dysfunctional cellular components. Autophagy allows the degradation and recycling of damaged proteins and organelles into their basic constituents of amino acids and fatty ... ...

    Abstract Autophagy is a vital cellular mechanism that controls the removal of damaged or dysfunctional cellular components. Autophagy allows the degradation and recycling of damaged proteins and organelles into their basic constituents of amino acids and fatty acids for cellular energy production. Under basal conditions, autophagy is essential for the maintenance of cell homeostasis and function. However, during cell stress, excessive activation of autophagy can be destructive and lead to cell death. Autophagy plays a crucial role in the cardiovascular system and helps to maintain normal cardiac function. During ischemia- reperfusion, autophagy can be adaptive or maladaptive depending on the timing and extent of activation. In this review, we highlight the molecular mechanisms and signaling pathways that underlie autophagy in response to cardiac stress and therapeutic approaches to modulate autophagy by pharmacological interventions. Finally, we also discuss the intersection between autophagy and circadian regulation in the heart. Understanding the mechanisms that underlie autophagy following cardiac injury can be translated to clinical cardiology use toward improved patient treatment and outcomes.
    MeSH term(s) Autophagy/drug effects ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Circadian Rhythm/drug effects ; Circadian Rhythm/physiology ; Humans ; Mitochondria/metabolism ; Myocardium/metabolism ; Polyphenols/pharmacology ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Polyphenols ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-01-20
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    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.2022.166354
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Editorial commentary: Mef2 regulated cardiac hypertrophy and heart failure in hypertension.

    Rabinovich-Nikitin, Inna / Kirshenbaum, Lorrie A

    Trends in cardiovascular medicine

    2022  Volume 33, Issue 4, Page(s) 213–214

    MeSH term(s) Humans ; Cardiomegaly/diagnosis ; Heart Failure/diagnosis ; Heart Failure/therapy ; Hypertension/diagnosis ; Myocytes, Cardiac
    Language English
    Publishing date 2022-01-31
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1097434-9
    ISSN 1873-2615 ; 1050-1738
    ISSN (online) 1873-2615
    ISSN 1050-1738
    DOI 10.1016/j.tcm.2022.01.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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