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Viral Infection and Apoptosis

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ISBN: 9783038426554 9783038426547 Year: Pages: 270 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-01-24 14:12:08
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Apoptosis is a form of programmed cell death that enables the removal of damaged, infected, or otherwise unwanted cells in a controlled manner. Apoptosis can be initiated by multiple independent pathways that ultimately converge at a point where proteolytic enzymes belonging to the caspase family are activated, which dismantle the apoptotic cell.Multicellular organism have employed apoptotic mechanisms during host defence in response to viral infection to limit or prevent viral spread and replication. Consequently, viruses have evolved sophisticated molecular countermeasures to disarm host apoptotic defences, and this series of reviews and primary research articles in this Special Issue explores the intricate molecular interplay between viruses and their hosts when they battle for control of host apoptotic check-points.

Keywords

Apoptosis --- caspase --- host defence

Chronic inflammation in conditions associated with a deficient clearance of dying and dead cells, their remnants, and intracellular constituents

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196012 Year: Pages: 73 DOI: 10.3389/978-2-88919-601-2 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-08-16 10:34:25
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In multicellular organisms, states with a high degree of tissue turnover like embryogenesis, development, and adult tissue homeostasis need an instantaneous, tightly regulated and immunologically silent clearance of these dying cells to ensure appropriate development of the embryo and adult tissue remodelling. The proper and swift clearance of apoptotic cells is essential to prevent cellular leakage of damage associated molecular patterns (DAMPs) which would lead to the stimulation of inflammatory cytokine responses. In addition to the clearance of apoptotic cells (efferocytosis), backup mechanisms are required to cope with DAMPs (HMGB-1, DNA, RNA, S100 molecules, ATP and adenosine) and other intracellular material (uric acid, intracellular proteins and their aggregates) released from cells, that were not properly cleared and have entered the stage of secondary necrosis. Furthermore, under certain pathologic conditions (e.g. gout, cancer, diabetes) non-apoptotic cell death may transiently occur (NETosis, necroptosis, pyroptosis) which generates material that also has to be cleared to avoid overloading tissues with non-functional cellular waste. Efficient efferocytosis is therefore indispensable for normal tissue turnover and homeostasis. The characterization of various signalling pathways that regulate this complex and evolutionary conserved process has shed light on new pathogenetic mechanisms of many diseases. Impaired clearance promotes initiation of autoimmunity as well as the perpetuation of chronic inflammation, but may also foster anti-tumor immunity under certain microenvironmental conditions. Immunological tolerance is continuously being challenged by the presence of post-apoptotic remnants in peripheral lymphoid tissues. Besides the autoimmune phenotype of chronic inflammatory rheumatoid disorders a plethora of pathologies have been associated with defects in genes involved in clearance, e.g. atherosclerosis, cancer, gout, diabetes, some forms of blindness, neuropathy, schizophrenia and Alzheimer’s disease. The main goal of this research topic is to collect contributions from various disciplines committed to studying pathogenetic mechanisms of the aforementioned disorders and dealing with alterations in the clearance of dying and dead cells, their remnants, and their constituents that leak out after membrane rupture. Integrating the combined collection of knowledge on efferocytosis and clearance of dead cells and their derived waste from different fields of research in physiology and pathophysiology could improve the molecular understanding of these increasingly prevalent diseases and may ultimately result in new therapeutic strategies.

Microbial Modulation of Host Apoptosis and Pyroptosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192809 Year: Pages: 109 DOI: 10.3389/978-2-88919-280-9 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Infectious disease is the result of an interactive relationship between a microbial pathogen and its host. In this interaction both the host and the pathogen attempt to manipulate each other using a complex network to maximize their respective survival probabilities. Programmed host cell death is a direct outcome of host-pathogen interaction and may benefit host or pathogen depending on microbial pathogenesis. Apoptosis and pyroptosis are two common programmed cell death types induced by various microbial infections. Apoptosis is non-inflammatory programmed cell death and can be triggered through intrinsic or extrinsic pathways and with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 after its activation by various inflammasomes. However, some non-canonical caspase-1-independent proinflammatory cell death phenomena have been reported. Microbial pathogens are able to modulate host apoptosis and pyroptosis through different triggers and pathways. The promotion and inhibition of host apoptosis and pyroptosis vary and depend on the microbe types, virulence, and phenotypes. For example, virulent pathogens and attenuated vaccine strains may use different pathways to modulate host cell death. Specific microbial genes may be responsible for the modulation of host cell death. Different host cells, including macrophages, dendritic cells, and T cells, can undergo apoptosis and pyroptosis after microbial infections. The pathways of host apoptosis and pyroptosis induced by different microbes may also differ. Different methods can be used to study the interaction between microbes and host cell death system. The articles included in this E-book report the cutting edge findings in the areas of microbial modulation of host apoptosis, pyroptosis and inflammasome.

Molecular mechanisms of cellular stress responses in cancer and their therapeutic implications

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194964 Year: Pages: 159 DOI: 10.3389/978-2-88919-496-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2015-11-16 15:44:59
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In response to stress, cells can activate a myriad of signalling pathways to bring about a specific cellular outcome, including cell cycle arrest, DNA repair, senescence and apoptosis. This response is pivotal for tumour suppression as all of these outcomes result in restriction of the growth and/or elimination of damaged and pre-malignant cells. Thus, a large number of anti-cancer agents target specific components of stress response signalling pathways with the aim of causing tumour regression by stimulating cell death. However, the efficacy of these agents is often impaired due to mutations in genes that are involved in these stress-responsive signalling pathways and instead the oncogenic potential of a cell is increased leading to the initiation and/or progression of tumourigenesis. Moreover, these genetic defects can increase or contribute to resistance to chemotherapeutic agents and/or radiotherapy. Modulating the outcome of cellular stress responses towards cell death in tumour cells without affecting surrounding normal cells is thus one of the ultimate aims in the development of new cancer therapeutics. To achieve this aim, a detailed understanding of cellular stress response pathways and their aberrations in cancer is required.This Research topic aims to reflect the broadness and complexity of this important area of cancer research.

Experimental models of early exposure to alcohol: a way to unravel the neurobiology of mental retardation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194728 Year: Pages: 104 DOI: 10.3389/978-2-88919-472-8 Language: English
Publisher: Frontiers Media SA
Subject: Pediatrics --- Psychiatry --- Medicine (General)
Added to DOAB on : 2016-03-10 08:14:33
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Excessive alcohol drinking represents a major social and public health problem for several countries. Alcohol abuse during pregnancy leads to a complex syndrome referred to as fetal alcohol spectrum disorders (FASD), chiefly characterized by mental retardation. The effects of early exposure to ethanol can be reproduced in laboratory animals and this helped to answer several key questions concerning the human pathology. The interest of experimental models of FASD is twofold. First, they increase our knowledge about the dose and modality of alcohol consumption able to induce damaging effects on the developing brain. Second, experimental models of FASD can provide useful hints to elucidate the basic mechanisms leading to the intellectual disability. In fact, experimental exposure to alcohol can be carried out during discrete, often very restricted, time windows. As a consequence, FASD models, though depending on the multifaceted interference of alcohol with several molecular pathways, can provide valuable information about which specific developmental periods and brain areas are critically involved in the genesis of mental retardation. Putting together data obtained through several experimental paradigms of alcohol exposure and those deriving from other genetic and non-genetic models, one can figure out to what extent different types of mental retardation share common pathogenetic mechanisms. The present Research Topic is aimed at establishing the state of the art of the current research on experimental FASD, focusing on differences and homologies with other types of intellectual disability. The ultimate goal is to find out a common roadmap in view of future therapeutical approaches.

Chemically-Induced DNA Damage, Mutagenesis, and Cancer

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ISBN: 9783038971290 9783038971306 Year: Pages: X, 264 Language: Englisch
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-08-27 13:43:27
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Human cancers frequently arise from exposure to chemicals, although radiation, oxidation, and genetic factors play critical roles as well. DNA damage by these agents in a cell is an important first step in the process of carcinogenesis. DNA repair processes have evolved to repair these damages. However, the replication of damaged DNA may occur frequently prior to repair, resulting in gene mutations and the generation of altered proteins. Mutations in an oncogene, a tumor-suppressor gene, or a gene that controls the cell cycle give rise to a clonal cell population with an advantage in proliferation. The complex process of carcinogenesis includes many such events, but has been generally considered to be comprised of the three main stages known as initiation, promotion, and progression, which ultimately give rise to the induction of human cancer. The articles published in this book entitled “Chemically-Induced DNA Damage, Mutagenesis, and Cancer” provide an overview on the topic of the “consequence of DNA damage” in the context of human cancer with their challenges and highlights.

Apoptotic Cell Clearance in Health and Disease

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456888 Year: Pages: 294 DOI: 10.3389/978-2-88945-688-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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Clearance of apoptotic cells is essential for proper development, homeostasis and termination of immune responses in multicellular organisms. Thus, cellular and molecular players taking part in the sequential events of this process are of great interest. Research in the last 20 years has indicated that specific ligands and receptors take part in the attraction of immune cells toward apoptotic targets and in the interactions between apoptotic cells and professional as well as non-professional phagocytes that engulf them. Moreover, phagocytosis of apoptotic cells (efferocytosis) leads to significant phenotypic changes in the engulfing cells suggesting that it is a major fate-determining event for phagocytes. Particularly, efferocytosis has an important impact on the inflammation-resolution axis as well as embryonic development and tissue morphogenesis. Deficiencies in these processes can result in health threats, such as autoimmunity, atherosclerosis, bone loss, obesity, infertility, neurodegeneration, fibrosis and cancer. This eBook brings together 24 original research and review manuscripts that cover various aspects of apoptotic cell removal during normal development and homeostasis as well as in tumorigenesis and regenerative processes following injury.

The changing faces of glutathione, a cellular protagonist

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195954 Year: Pages: 142 DOI: 10.3389/978-2-88919-595-4 Language: English
Publisher: Frontiers Media SA
Subject: Therapeutics --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Glutathione (GSH) has been described for a long time just as a defensive reagent against the action of toxic xenobiotics (drugs, pollutants, carcinogens), both directly and as a cofactor for GSH transferases. As a prototype antioxidant, it has been involved in cell protection from the noxious effect of excess oxidant stress, both directly and as a cofactor of glutathione peroxidases. In addition, it has long been known that GSH is capable of forming disulfide bonds with cysteine residues of proteins, and the relevance of this mechanism ("S-glutathionylation") in regulation of protein function has been well documented in a number of research fields. Rather paradoxically, it has also been highlighted that GSH—and notably its catabolites, as originated by metabolism by gamma-glutamyltransferase—can promote oxidative processes, by participating in metal ion-mediated reactions eventually leading to formation of reactive oxygen species and free radicals. Also, a fundamental role of GSH has been recognized in the storage and transport of nitric oxide (NO), in the form of S-nitrosoglutathione (GSNO). The significance of GSH as a major factor in regulation of cell life, proliferation, and death, can be regarded as the integrated result of all these roles, as well as of more which are emerging in diverse fields of biology and pathophysiology. Against this background, modulation of GSH levels and GSH-related enzyme activities represents a fertile field for experimental pharmacology in numerous and diverse perspectives of animal, plant and microbiologic research. This research topic includes 14 articles, i.e. 4 Opinion Articles, 6 Reviews, and 4 Original Research Articles. The contributions by several distinguished research groups, each from his own standpoint of competence and expertise, provide a comprehensive and updated view over the diverse roles, the changing faces of GSH and GSH-related enzymes in cell’s health, disease and death.

Pathophysiological Mechanisms of Sarcopenia in Aging and in Muscular Dystrophy: A Translational Approach

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196845 Year: Pages: 248 DOI: 10.3389/978-2-88919-684-5 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Loss of muscle mass and increased fibrosis characterize both sarcopenia of aging and muscular dystrophy. Research is increasingly showing that these two conditions also share several pathophysiological mechanisms, including mitochondrial dysfunction, increased apoptosis, abnormal modulation of autophagy, decline in satellite cells, increased generation of reactive oxygen species, and abnormal regulation of signaling and stress response pathways. This Research Topic will cover several mechanisms involved in aging and dystrophic sarcopenia and explore the therapeutic potential of various strategies for intervention.

Translocator Protein (TSPO)

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ISBN: 9783038427575 9783038427582 Year: Pages: 176 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-03-16 13:21:14
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The high number of papers submitted and ultimately accepted for publication in this special issue attests the great amount of research being conducted on TSPO and its role in living cells. Thus, TSPO has become an extremely attractive subcellular biomark for the early detection of disease states overexpressing this protein and for the selective delivery to mitochondria of drugs and probes. Moreover, the effort in the design and synthesis of new, more specific and effective TSPO ligands proves to be very valuable. All these topics have been addressed in the special issue.

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