Crosstalk between Cell Death, Oxidative Stress, and Immune Regulation PDF Download
Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download Crosstalk between Cell Death, Oxidative Stress, and Immune Regulation PDF full book. Access full book title Crosstalk between Cell Death, Oxidative Stress, and Immune Regulation by Chao Yang. Download full books in PDF and EPUB format.
Author: Chao Yang
Publisher: Frontiers Media SA
ISBN: 2832556647
Category : Medical
Languages : en
Pages : 182
Get Book Here
Book Description
Cell death, a biological event important for maintaining the growth, development, and life processes of organisms, mainly includes programmed death (apoptosis, pyroptosis, autophagy, mitochondrial apoptosis, ferroptosis, cuproptosis, and disulfidptosis, etc.) and non-programmed death (cell necrosis). Many diseases, including cancers, exhibit dysregulated immune activities as key features due to the increase in oxidative stress, which eventually leads to cell death. Understanding the intricate relationships between cell death, oxidative stress, and immune regulation could be critical in elucidating the key molecular mechanisms of these diseases, possibly uncovering novel therapeutics/diagnostics for disease management. For example, ferroptosis, a form of iron-dependent cell death that is triggered by the toxic accumulation of oxidative stress, can induce immunosuppression in tumor neutrophils, whereas inhibition of ferroptosis can slow tumor progression. For another example, pyroptosis, a form of lytic cell death which can be triggered by oxidative stress, when occurs in tumor cells, can induce a strong inflammatory response and significant tumor regression.
Author: Chao Yang
Publisher: Frontiers Media SA
ISBN: 2832556647
Category : Medical
Languages : en
Pages : 182
Get Book Here
Book Description
Cell death, a biological event important for maintaining the growth, development, and life processes of organisms, mainly includes programmed death (apoptosis, pyroptosis, autophagy, mitochondrial apoptosis, ferroptosis, cuproptosis, and disulfidptosis, etc.) and non-programmed death (cell necrosis). Many diseases, including cancers, exhibit dysregulated immune activities as key features due to the increase in oxidative stress, which eventually leads to cell death. Understanding the intricate relationships between cell death, oxidative stress, and immune regulation could be critical in elucidating the key molecular mechanisms of these diseases, possibly uncovering novel therapeutics/diagnostics for disease management. For example, ferroptosis, a form of iron-dependent cell death that is triggered by the toxic accumulation of oxidative stress, can induce immunosuppression in tumor neutrophils, whereas inhibition of ferroptosis can slow tumor progression. For another example, pyroptosis, a form of lytic cell death which can be triggered by oxidative stress, when occurs in tumor cells, can induce a strong inflammatory response and significant tumor regression.
Author: Anne Le
Publisher: Springer
ISBN: 331977736X
Category : Medical
Languages : en
Pages : 186
Get Book Here
Book Description
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
Author: Robert Clarke
Publisher: Springer
ISBN: 303005067X
Category : Medical
Languages : en
Pages : 227
Get Book Here
Book Description
This volume presents state-of-the-art information on each of the arms of the unfolded protein response (UPR), how their activation/repression are regulated, integrated, and coordinated, how UPR components affect cancer cell biology and responsiveness to therapeutic interventions, and how UPR components/activities offer potentially novel targets for drug discovery, repurposing, and development. The volume will provide the most recent information on the signaling and regulation of the UPR, explore examples of how the UPR and/or specific components contribute to cancer biology, and identify and explore specific examples of potently new actionable targets for drug discovery and development from within the UPR and its regulation. Unique to the volume will be a specific focus on the UPR and its role in cancer biology, as well as a discussion of the role of the UPR in drug responses and resistance in cancer.
Author: Han-Ming Shen
Publisher: Springer Science & Business Media
ISBN: 1461482208
Category : Science
Languages : en
Pages : 402
Get Book Here
Book Description
Starting with discussion of basic concepts and the molecular mechanisms of necrosis, this book looks first at several forms of necrotic cell death that have been identified, including necroptosis, autophagic cell death, and PARP-mediated cell death. As necrotic cell death is increasingly known to play a critical role in many physiological processes, the next chapters discuss its effect on metabolism, inflammation, immunity, and development. Necrotic cell death is closely implicated in human diseases like cancer, so the next chapters examine its relevance to human diseases, and final chapters cover methodologies for measuring necrosis. This book presents comprehensive coverage of necrosis from recognized experts from leading academic and medical institutions around the world. In contrast to apoptosis, well-defined as a form of programmed cell death, necrosis used to be considered as accidental (i.e., non-programmed) cell death, usually in response to a severe injury. Accumulating evidence now suggests, however, that necrosis is also programmed and controlled by distinctive "death machinery" in response to various stimuli like oxidative stress or DNA damage.
Author: Tamas Fulop
Publisher: Springer Science & Business Media
ISBN: 1402090633
Category : Medical
Languages : en
Pages : 1693
Get Book Here
Book Description
This authoritative handbook covers all aspects of immunosenescence, with contributions from experts in the research and clinical areas. It examines methods and models for studying immunosenescence; genetics; mechanisms including receptors and signal transduction; clinical relevance in disease states including infections, autoimmunity, cancer, metabolic syndrome, neurodegenerative diseases, frailty and osteoporosis; and much more.
Author: Guy C. Brown
Publisher:
ISBN:
Category : Cell death
Languages : en
Pages : 248
Get Book Here
Book Description
Author: Hong-Gang Wang
Publisher: Springer Science & Business Media
ISBN: 1461465613
Category : Medical
Languages : en
Pages : 267
Get Book Here
Book Description
With the explosion of information on autophagy in cancer, this is an opportune time to speed the efforts to translate our current knowledge about autophagy regulation into better understanding of its role in cancer. This book will cover the latest advances in this area from the basics, such as the molecular machinery for autophagy induction and regulation, up to the current areas of interest such as modulation of autophagy and drug discovery for cancer prevention and treatment. The text will include an explanation on how autophagy can function in both oncogenesis and tumor suppression and a description of its function in tumor development and tumor suppression through its roles in cell survival, cell death, cell growth as well as its influences on inflammation, immunity, DNA damage, oxidative stress, tumor microenvironment, etc. The remaining chapters will cover topics on autophagy and cancer therapy. These pages will serve as a description on how the pro-survival function of autophagy may help cancer cells resist chemotherapy and radiation treatment as well as how the pro-death functions of autophagy may enhance cell death in response to cancer therapy, and how to target autophagy for cancer prevention and therapy − what to target and how to target it.
Author: Zahra Zakeri
Publisher:
ISBN:
Category : Science
Languages : en
Pages : 236
Get Book Here
Book Description
Contains papers from a July 1998 conference held at the Queens College Campus of the City University of New York. Papers are arranged in sections on mechanisms and general considerations, programmed (developmental) cell death, and cell death and pathological and clinical situations. Specific topics
Author:
Publisher: BoD – Books on Demand
ISBN: 1838801251
Category : Science
Languages : en
Pages : 140
Get Book Here
Book Description
The imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses determines a state known as oxidative stress. Higher levels of pro-oxidants compared to antioxidant defenses may generate oxidative damage, which, in turn, may lead to modifications in cellular proteins, lipids, and DNA, reducing functional capacity and increasing the risk of diseases. Nevertheless, the clearance of harmful reactive chemical species is achieved by the antioxidant defense systems. These protection systems are referred to as the first and second lines of defense and comprise the classic antioxidants, enzymatic and nonenzymatic defenses, including glutathione. This book presents and discusses the advancement of research on health and diseases and their underlying mechanisms, exploring mainly aspects related to the glutathione antioxidant system.
Author: Hans J. Bremer
Publisher: Urban & Schwarzenberg
ISBN:
Category : Medical
Languages : en
Pages : 552
Get Book Here
Book Description
