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001442967 020__ $$a9783030787998$$q(electronic bk.)
001442967 020__ $$a3030787990$$q(electronic bk.)
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001442967 0247_ $$a10.1007/978-3-030-78799-8$$2doi
001442967 035__ $$aSP(OCoLC)1286950579
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001442967 049__ $$aISEA
001442967 050_4 $$aQH671
001442967 08204 $$a571.9/36$$223
001442967 24500 $$aBiochemistry of apoptosis and autophagy /$$cLorrie A. Kirshenbaum, editor.
001442967 260__ $$aCham, Switzerland :$$bSpringer,$$c[2022]
001442967 300__ $$a1 online resource
001442967 336__ $$atext$$btxt$$2rdacontent
001442967 337__ $$acomputer$$bc$$2rdamedia
001442967 338__ $$aonline resource$$bcr$$2rdacarrier
001442967 347__ $$atext file
001442967 347__ $$bPDF
001442967 4901_ $$aAdvances in biochemistry in health and disease ;$$vv. 18
001442967 5050_ $$aA Protein-centric Perspective of Autophagy and Apoptosis Signaling and Crosstalk in Health and Disease -- Adrenergic receptor signaling pathways in the regulation of apoptosis -- Apoptosis in Ischemic Heart Disease -- Autophagy in cardiac physiology and pathology -- Caspase signaling pathways as convenors of stress adaptation -- Cross talk between apoptosis and autophagy in regulating the progression of heart disease -- Fibroblasts, Fibrosis and Autophagy -- Gene Therapy and Its Application In Cardiac Diseases -- Inflammation and mitochondrial degradation in the heart -- Mitochondria and Cellular Hosts_An Uneasy Truce -- Mitochondrial Dysfunction and Mitophagy -- Proteotoxicity and Autophagy in Neurodegenerative and Cardiovascular Diseases -- Regulation of Cell Death Signaling Pathways in Cardiac Myocytes by Mitochondrial Bnip3 Inna -- Role of Cardiomyocyte Apoptosis in Heart Failure -- The Role of FGF2 Isoforms In Cell Survival In The Heart.
001442967 506__ $$aAccess limited to authorized users.
001442967 520__ $$aOne of the most intriguing and compelling issues to impact contemporary biology to date is the concept that cell death is genetically regulated. Observations by Kerr and Wyllie, made more than 30 years ago on the basis of distinct morphological criteria, markedly distinguished apoptosis from classical cell death by necrosis. Apoptosis is a highly regulated, evolutionary conserved, genetic program of cell death essential for normal development and tissue homeostasis. The discovery of apoptosis as a regulated event and potentially amenable to therapeutic interventions has generated considerable excitement because it meant that disease entities resulting from either too much, or too little, apoptosis could be potentially cured with new therapies that target apoptosis. While there is little doubt that necrosis induced by massive cellular trauma is likely an unregulated event, several lines of investigation have challenged the dogma that necrotic cell death is merely unregulated. Emerging data has shifted the paradigm in our thinking about necrosis as a regulated event. Autophagy is another cellular process that has received considerable attention over the past two decades and its remarkable involvement in the processes of cell survival, death and tumorigenesis. Macro autophagy is a catabolic process that involves the selective and targeted removal of oxidized proteins, macromolecular structures and organelles through an elaborate cellular process involving a lysosome mediated pathway. Other forms of autophagy involving adapter proteins, commonly referred to as chaperone mediated autophagy, involves the selective removal of cellular cargo by the ubiquitin-proteasome pathway. The book will serve as a reference guide for basic and clinical scientists who are interested in understanding how these critical cellular processes impact the pathogenesis of human disease.
001442967 588__ $$aOnline resource; title from PDF title page (SpringerLink, viewed December 20, 2021).
001442967 650_0 $$aCell death.
001442967 650_6 $$aCellules$$xMort.
001442967 655_0 $$aElectronic books.
001442967 7001_ $$aKirshenbaum, Lorrie A.,$$eeditor.
001442967 77608 $$iPrint version:$$z3030787982$$z9783030787981$$w(OCoLC)1250512738
001442967 830_0 $$aAdvances in biochemistry in health and disease ;$$vv. 18.
001442967 852__ $$bebk
001442967 85640 $$3Springer Nature$$uhttps://univsouthin.idm.oclc.org/login?url=https://link.springer.com/10.1007/978-3-030-78799-8$$zOnline Access$$91397441.1
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001442967 983__ $$aOnline
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