標(biāo)題: Titlebook: Biochemistry of Apoptosis and Autophagy; Lorrie A. Kirshenbaum Book 2022 Springer Nature Switzerland AG 2022 Apoptosis.Autophagy.Cell Deat [打印本頁(yè)] 作者: 帳簿 時(shí)間: 2025-3-21 17:15
書(shū)目名稱Biochemistry of Apoptosis and Autophagy影響因子(影響力)
書(shū)目名稱Biochemistry of Apoptosis and Autophagy影響因子(影響力)學(xué)科排名
書(shū)目名稱Biochemistry of Apoptosis and Autophagy網(wǎng)絡(luò)公開(kāi)度
書(shū)目名稱Biochemistry of Apoptosis and Autophagy網(wǎng)絡(luò)公開(kāi)度學(xué)科排名
書(shū)目名稱Biochemistry of Apoptosis and Autophagy被引頻次
書(shū)目名稱Biochemistry of Apoptosis and Autophagy被引頻次學(xué)科排名
書(shū)目名稱Biochemistry of Apoptosis and Autophagy年度引用
書(shū)目名稱Biochemistry of Apoptosis and Autophagy年度引用學(xué)科排名
書(shū)目名稱Biochemistry of Apoptosis and Autophagy讀者反饋
書(shū)目名稱Biochemistry of Apoptosis and Autophagy讀者反饋學(xué)科排名
作者: 甜食 時(shí)間: 2025-3-21 21:58
978-3-030-78801-8Springer Nature Switzerland AG 2022作者: 舔食 時(shí)間: 2025-3-22 03:23
Lorrie A. KirshenbaumCovers all aspects of apoptosis.Chapters submitted from world renowned researchers.Unique in defining the relationship between the regulatory mechanisms作者: Evolve 時(shí)間: 2025-3-22 06:22
Advances in Biochemistry in Health and Diseasehttp://image.papertrans.cn/b/image/186692.jpg作者: 妨礙 時(shí)間: 2025-3-22 09:17 作者: congenial 時(shí)間: 2025-3-22 16:07 作者: 禁止,切斷 時(shí)間: 2025-3-22 20:00 作者: 手段 時(shí)間: 2025-3-22 23:00
https://doi.org/10.1007/978-3-322-90036-4rodents. Individual cardiomyocytes are thus quite long-lived and must be able to continuously adapt to physiologic and pathophysiologic stresses. Stress adaptation often entails the renewal of intracellular constituents, as exemplified by the changes in enzymatic activity which accompanies shifts in作者: Mangle 時(shí)間: 2025-3-23 04:03 作者: 協(xié)定 時(shí)間: 2025-3-23 07:36 作者: HUMID 時(shí)間: 2025-3-23 10:02
https://doi.org/10.1007/978-3-322-90036-4scarring if sufficiently excessive. Fibrosis affects many tissue types, and thus contributes to a broad group of diseases which, with few exceptions, continues to lack specific therapy. It has been estimated that nearly 45% of deaths in the developed world are caused by fibroproliferative diseases, 作者: 皮薩 時(shí)間: 2025-3-23 16:54
Hans Joachim Salize,Wulf R?sslerbrosis, myocardial infarction, arrhythmias, and cardiomyopathies leading to cardiac dysfunction and heart failure remain significant contributors to this problem. For decades, therapeutic intervention has relied almost exclusively on surgical or pharmacologic approaches, and while these have improve作者: DOLT 時(shí)間: 2025-3-23 19:20 作者: Allergic 時(shí)間: 2025-3-23 23:04
Kosten und Leistungen von Baumaschinens review we discuss the interplay between mitochondria and the cells they occupy. Cells regulate the potentially lethal aspects of mitochondria by inserting both pro-apoptotic and anti-apoptotic machinery into mitochondria. In this way mitochondria can trigger apoptosis, ferroptosis, necrosis, and e作者: Fatten 時(shí)間: 2025-3-24 05:00
Kosten und Leistungen von Baumaschinenxcess loss of cardiac myocytes and increased fibrosis, which leads to a reduced capacity to sustain contractile function. Cardiac myocytes are highly enriched in mitochondria which are responsible for generating energy via oxidative phosphorylation. Although mitochondria are critical for myocyte fun作者: ICLE 時(shí)間: 2025-3-24 09:23
Berechnung der Durchschnittskosten particular, protein aggregation has been implicated in several neurodegenerative and cardiovascular diseases, such as Alzheimer’s disease and cardiac amyloidosis, that are associated with significant morbidity and mortality. Increasing evidence highlights that misfolded protein oligomers exert sign作者: Reservation 時(shí)間: 2025-3-24 14:02 作者: Frenetic 時(shí)間: 2025-3-24 18:08 作者: 涂掉 時(shí)間: 2025-3-24 22:15
https://doi.org/10.1007/978-3-663-08128-9n made, there remain a need to identify additional strategies to manage heart disease and improve outcomes. Identifying the various signals and pathways that contribute to cardiac cell pathology and death, as well as those that promote cell survival and overall protection can lead to new ways to int作者: 浪蕩子 時(shí)間: 2025-3-25 00:18 作者: Ambiguous 時(shí)間: 2025-3-25 05:29
Book 2022f investigation have challenged the dogma that necrotic cell death ismerely 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 remark作者: 避開(kāi) 時(shí)間: 2025-3-25 09:56
A Protein-Centric Perspective of Autophagy and Apoptosis Signaling and Crosstalk in Health and Disees. This book chapter focuses on delineating critical promoters of these two distinct biological processes as well as their interdependent molecular crosstalk from a protein-centric perspective. To better appreciate their clinical relevance, we also highlight the role of autophagy, apoptosis, and th作者: hermitage 時(shí)間: 2025-3-25 14:10 作者: Cholagogue 時(shí)間: 2025-3-25 19:16 作者: reflection 時(shí)間: 2025-3-25 21:50 作者: 諂媚于性 時(shí)間: 2025-3-26 02:23
Cross Talk Between Apoptosis and Autophagy in Regulating the Progression of Heart Disease,n signaling pathways. Therefore, the interaction of proteins specific to autophagy with the apoptotic proteins might result in activation or inactivation of the process. This chapter summarizes mechanisms of both the pathways in cardiomyocytes and the molecules that link these pathways to regulate c作者: Flat-Feet 時(shí)間: 2025-3-26 08:03 作者: Chronic 時(shí)間: 2025-3-26 09:20
Gene Therapy and Its Application in Cardiac Diseases,comes severely limited adoption. Improvements in gene therapeutic approaches have resulted in safer and more precisely-targeted means of treating heart diseases, with considerable advancement in the field in recent years. In this chapter, we review the viral and non-viral vectors which have been uti作者: 揉雜 時(shí)間: 2025-3-26 13:05 作者: Immobilize 時(shí)間: 2025-3-26 20:13 作者: 致命 時(shí)間: 2025-3-27 00:21
Role of Cardiomyocyte Apoptosis in Heart Failure,to show the role of TNF-α in the activation and deactivation of cell survival and cell death signal transduction pathways for the occurrence of apoptosis in non-ischemic failing hearts due to volume overload and dilated cardiomyopathy. Although the occurrence of apoptosis in failing hearts can be se作者: 刺耳 時(shí)間: 2025-3-27 04:03
,The Role of FGF2 isoforms?in Cell Survival in the Heart,ell types but especially cardiac cells. Our focus will be on molecular signals associated with the causation of, or prevention from, various forms of cells death, by apoptosis, necrosis and dysregulated autophagy, and their relationship to different FGF2 isoforms. In the second part we will present 作者: 浪蕩子 時(shí)間: 2025-3-27 05:49
Erwin Grochla,Helmut Weber,Thomas Werhahnes. This book chapter focuses on delineating critical promoters of these two distinct biological processes as well as their interdependent molecular crosstalk from a protein-centric perspective. To better appreciate their clinical relevance, we also highlight the role of autophagy, apoptosis, and th作者: hermetic 時(shí)間: 2025-3-27 10:12 作者: Fibroid 時(shí)間: 2025-3-27 16:47 作者: fulmination 時(shí)間: 2025-3-27 19:21 作者: 車(chē)床 時(shí)間: 2025-3-28 01:39 作者: Canopy 時(shí)間: 2025-3-28 04:58 作者: Hemiplegia 時(shí)間: 2025-3-28 08:01 作者: 束以馬具 時(shí)間: 2025-3-28 13:21
Kosten und Leistungen von Baumaschinenntity and is critical for maintaining a healthy population of mitochondria. Defects in this process affect cardiac homeostasis and contribute to cardiac aging and development of various myocardial pathologies. This chapter provides insights into the molecular mechanisms involved in regulating mitoph作者: Cloudburst 時(shí)間: 2025-3-28 18:04
Berechnung der Durchschnittskostenameliorate the end organ damage caused by protein aggregates. Therefore, understanding the interactions between protein aggregation and autophagy are crucial to treat proteotoxic neurodegenerative and cardiovascular diseases.作者: Ostrich 時(shí)間: 2025-3-28 22:16
,Prim?reffekt durch Investitionen,to show the role of TNF-α in the activation and deactivation of cell survival and cell death signal transduction pathways for the occurrence of apoptosis in non-ischemic failing hearts due to volume overload and dilated cardiomyopathy. Although the occurrence of apoptosis in failing hearts can be se作者: 打谷工具 時(shí)間: 2025-3-29 02:26 作者: Visual-Acuity 時(shí)間: 2025-3-29 06:35 作者: Choreography 時(shí)間: 2025-3-29 09:37
Kosten- und Zeitbegriffe der Bauger?telistenction. Herein, we review the relevant literature highlighting the interworking of circadian interaction with metabolism including nutrient stress and autophagy within the cardiovascular system. We hope to use this information to spark interest in the potential for circadian intervened therapies designed for improving cardiovascular metabolism.作者: Carcinogenesis 時(shí)間: 2025-3-29 14:37 作者: 勾引 時(shí)間: 2025-3-29 16:53
Circadian Regulation of Autophagy in the Heart Via the mTOR Pathway,ction. Herein, we review the relevant literature highlighting the interworking of circadian interaction with metabolism including nutrient stress and autophagy within the cardiovascular system. We hope to use this information to spark interest in the potential for circadian intervened therapies designed for improving cardiovascular metabolism.作者: 單片眼鏡 時(shí)間: 2025-3-29 23:20
Regulation of Cell Death Signaling Pathways in Cardiac Myocytes by Mitochondrial Bnip3,t importance toward developing new therapies to modulate cardiac cell death during cell stress conditions. Herein, we highlight the role of Bnip3 in cardiac cell death under two physiologically important and clinically relevant conditions where Bnip3 is known to be activated, namely ischemic stress and doxorubicin cardiotoxicity.作者: genuine 時(shí)間: 2025-3-30 03:46
Mitochondria and Their Cell Hosts: Best of Frenemies,nergy insufficiency; they also serve as a nexus for inflammatory signaling. Cellular mitigation of mitochondrial mischief includes anti-apoptotic Bcl-2 family members, mitophagy and other protein quality control mechanisms. 作者: BUDGE 時(shí)間: 2025-3-30 05:15 作者: 濕潤(rùn) 時(shí)間: 2025-3-30 10:59 作者: CESS 時(shí)間: 2025-3-30 14:30
2512-2142 y mechanismsOne 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 作者: 下船 時(shí)間: 2025-3-30 18:11
https://doi.org/10.1007/978-3-322-90036-4aspases in cell differentiation and stress adaptation, and the evolution of nonapoptotic activity of these proteases and related factors. We also discuss how caspases integrate other cell death signaling pathways to manage and guide stress response in the mammalian heart, independent of cell death.作者: 爵士樂(lè) 時(shí)間: 2025-3-30 23:08
Caspase Signaling Pathways as Convenors of Stress Adaptation,aspases in cell differentiation and stress adaptation, and the evolution of nonapoptotic activity of these proteases and related factors. We also discuss how caspases integrate other cell death signaling pathways to manage and guide stress response in the mammalian heart, independent of cell death.作者: 殖民地 時(shí)間: 2025-3-31 03:07 作者: Regurgitation 時(shí)間: 2025-3-31 06:35 作者: Hearten 時(shí)間: 2025-3-31 10:03
Apoptosis in Ischemic Heart Disease,ed with irreversible cellular damage and contractile failure. Although several major mechanisms including inflammation, oxidative stress and intracellular Ca.-overload have been identified to induce cardiac injury in IHD, the occurrence of cardiomyocyte cell death due to apoptosis has been considere
