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This book is focused on the analysis of the role played by immune cell components in the angiogenic process associated with inflammation and tumor growth. Both innate and adaptive immune cells are involved in the mechanisms of endothelial cell proliferation, migration and activation, through the production and release of a large spectrum of pro-angiogenic mediators. These may create the specific microenvironment that favors an increased rate of tissue vascularization. The link between chronic inflammation and tumorigenesis was first proposed by Rudolf Virchow in 1863 after the observation that infiltrating leukocytes are a hallmark of tumors and first established a causative connection between the lymph reticular infiltrate at sites of chronic inflammation and the development of cancer. Tumors were described as wounds that never heal and surgeons have long described the tendency of tumors to recur in healing resection margin and it has been reported that wound healing environment provides an opportunistic matrix for tumor growth. As angiogenesis is the result of a net balance between the activities exerted by positive and negative regulators, this book will also provide information on some anti-angiogenic properties of immune cells that may be utilized for a potential pharmacological use as anti-angiogenic agents in inflammation as well as in cancer. The work is written for researchers in the field and also for graduate students which approach this matter.
Book Synopsis Inflammation and Angiogenesis by : Domenico Ribatti
Download or read book Inflammation and Angiogenesis written by Domenico Ribatti and published by Springer. This book was released on 2017-11-08 with total page 116 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is focused on the analysis of the role played by immune cell components in the angiogenic process associated with inflammation and tumor growth. Both innate and adaptive immune cells are involved in the mechanisms of endothelial cell proliferation, migration and activation, through the production and release of a large spectrum of pro-angiogenic mediators. These may create the specific microenvironment that favors an increased rate of tissue vascularization. The link between chronic inflammation and tumorigenesis was first proposed by Rudolf Virchow in 1863 after the observation that infiltrating leukocytes are a hallmark of tumors and first established a causative connection between the lymph reticular infiltrate at sites of chronic inflammation and the development of cancer. Tumors were described as wounds that never heal and surgeons have long described the tendency of tumors to recur in healing resection margin and it has been reported that wound healing environment provides an opportunistic matrix for tumor growth. As angiogenesis is the result of a net balance between the activities exerted by positive and negative regulators, this book will also provide information on some anti-angiogenic properties of immune cells that may be utilized for a potential pharmacological use as anti-angiogenic agents in inflammation as well as in cancer. The work is written for researchers in the field and also for graduate students which approach this matter.
The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
Book Synopsis Inflammation and the Microcirculation by : D. Neil Granger
Download or read book Inflammation and the Microcirculation written by D. Neil Granger and published by Morgan & Claypool Publishers. This book was released on 2010 with total page 99 pages. Available in PDF, EPUB and Kindle. Book excerpt: The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
This much-needed text develops current knowledge on the mechanisms of angiogenesis at the molecular and cellular levels as they relate to inflammation, including acute and chronic inflammation, neurogenic initiation, and the role of the multiple cellular components that comprise inflammation. The volume brings together experts in each of these fields to link the molecular and cellular processes in angiogenesis to those of inflammation and disease, culminating in a discourse on areas for future therapies.
Book Synopsis Angiogenesis in Inflammation: Mechanisms and Clinical Correlates by : Michael Seed
Download or read book Angiogenesis in Inflammation: Mechanisms and Clinical Correlates written by Michael Seed and published by Springer Science & Business Media. This book was released on 2008-11-14 with total page 187 pages. Available in PDF, EPUB and Kindle. Book excerpt: This much-needed text develops current knowledge on the mechanisms of angiogenesis at the molecular and cellular levels as they relate to inflammation, including acute and chronic inflammation, neurogenic initiation, and the role of the multiple cellular components that comprise inflammation. The volume brings together experts in each of these fields to link the molecular and cellular processes in angiogenesis to those of inflammation and disease, culminating in a discourse on areas for future therapies.
Inflammation and angiogenesis, the growth of new blood vessels from pre-existing ones, are involved in tumor growth, ocular diseases and wound healing. In ocular angiogenesis, new pathological vessels grow into a specific eye tissue, leak fluid, and disrupt vision. The development of safe and effective therapies for ocular angiogenesis is of great importance for preventing blindness, given that current treatments have limited efficacy or are associated with undesirable side effects. The search for alternative treatment targets requires a deeper understanding of inflammation and how it can lead to angiogenesis in the eye in pathologic situations. This thesis provides new insights into the regulation of inflammation and angiogenesis, particularly at the gene expression and phenotypic levels, in different situations characterized by angiogenesis of the cornea, often called corneal neovascularization. For instance, specific genes and pathways are either endogenously activated or suppressed during active inflammation, wound healing, and during resolution of inflammation and angiogenesis, serving as potential targets to modulate the inflammatory and angiogenic response. In addition, as part of the healing response to restore corneal transparency, inflammation and angiogenesis subside with time in the cornea. In this context, LXR/RXR signaling was found to be activated in a time-dependent manner, to potentially regulate resolution of inflammation and angiogenesis. During regression of new angiogenic capillaries, ghost vessels and empty basement membrane sleeves are formed, which can persist in the cornea for a long time. Here, ghost vessels were found to facilitate subsequent revascularization of the cornea, while empty basement membrane sleeves did not revascularize. The revascularization response observed here was characterised by vasodilation, increased inflammatory cell infiltration and by sprouting at the front of the reperfused vessels. Importantly, reactive oxygen species and nitrous oxide signaling among other pro-inflammatory pathways were activated, and at the same time anti-inflammatory LXR/RXR signaling was inhibited. The interplay between activation and inhibition of these pathways highlights potential mechanisms that regulate corneal revascularization. When treating corneal neovascularization clinically, corticosteroids are in widespread use due to their effectiveness. To minimize the many undesirable side effects associated with corticosteroid use, however, identifying new and more selective agents is of great importance. Here, it was observed that corticosteroids not only suppressed pro-inflammatory chemokines and cytokines, but also activated the classical complement pathway. Classical complement may represent a candidate for further selective therapeutic manipulation to investigate its effect on treatment of corneal neovascularization. In summary, this thesis identifies genes, pathways, and phenotypic responses involved in sprouting and remodeling of corneal capillaries, highlights novel pathways and factors that may regulate inflammation and angiogenesis in the cornea, and provides insights into regulation of capillary regression and reactivation. Further investigation of these regulatory mechanisms may offer alternative and effective treatment targets for the treatment of corneal inflammation and angiogenesis.
Book Synopsis Regulation of inflammation and angiogenesis in the cornea by : Anthony Mukwaya
Download or read book Regulation of inflammation and angiogenesis in the cornea written by Anthony Mukwaya and published by Linköping University Electronic Press. This book was released on 2018-05-21 with total page 55 pages. Available in PDF, EPUB and Kindle. Book excerpt: Inflammation and angiogenesis, the growth of new blood vessels from pre-existing ones, are involved in tumor growth, ocular diseases and wound healing. In ocular angiogenesis, new pathological vessels grow into a specific eye tissue, leak fluid, and disrupt vision. The development of safe and effective therapies for ocular angiogenesis is of great importance for preventing blindness, given that current treatments have limited efficacy or are associated with undesirable side effects. The search for alternative treatment targets requires a deeper understanding of inflammation and how it can lead to angiogenesis in the eye in pathologic situations. This thesis provides new insights into the regulation of inflammation and angiogenesis, particularly at the gene expression and phenotypic levels, in different situations characterized by angiogenesis of the cornea, often called corneal neovascularization. For instance, specific genes and pathways are either endogenously activated or suppressed during active inflammation, wound healing, and during resolution of inflammation and angiogenesis, serving as potential targets to modulate the inflammatory and angiogenic response. In addition, as part of the healing response to restore corneal transparency, inflammation and angiogenesis subside with time in the cornea. In this context, LXR/RXR signaling was found to be activated in a time-dependent manner, to potentially regulate resolution of inflammation and angiogenesis. During regression of new angiogenic capillaries, ghost vessels and empty basement membrane sleeves are formed, which can persist in the cornea for a long time. Here, ghost vessels were found to facilitate subsequent revascularization of the cornea, while empty basement membrane sleeves did not revascularize. The revascularization response observed here was characterised by vasodilation, increased inflammatory cell infiltration and by sprouting at the front of the reperfused vessels. Importantly, reactive oxygen species and nitrous oxide signaling among other pro-inflammatory pathways were activated, and at the same time anti-inflammatory LXR/RXR signaling was inhibited. The interplay between activation and inhibition of these pathways highlights potential mechanisms that regulate corneal revascularization. When treating corneal neovascularization clinically, corticosteroids are in widespread use due to their effectiveness. To minimize the many undesirable side effects associated with corticosteroid use, however, identifying new and more selective agents is of great importance. Here, it was observed that corticosteroids not only suppressed pro-inflammatory chemokines and cytokines, but also activated the classical complement pathway. Classical complement may represent a candidate for further selective therapeutic manipulation to investigate its effect on treatment of corneal neovascularization. In summary, this thesis identifies genes, pathways, and phenotypic responses involved in sprouting and remodeling of corneal capillaries, highlights novel pathways and factors that may regulate inflammation and angiogenesis in the cornea, and provides insights into regulation of capillary regression and reactivation. Further investigation of these regulatory mechanisms may offer alternative and effective treatment targets for the treatment of corneal inflammation and angiogenesis.
Metabolic Syndrome (MS) is a highly prevalent condition in developed countries and is a cluster of several risk factors for type 2 diabetes and cardiovascular disease that includes increased body mass index/waist circumference, visceral obesity, insulin resistance, hyperclycaemia, dyslipidaemia and hypertension, which are all major causes of morbidity and death. This volume provides a critical review and discussion of the knowledge gathered on MS and analyzes the interplay between oxidative stress, chronic inflammation and angiogenesis features. There is a special focus on recent discoveries and progress toward possible therapeutic strategies, such as the role of glucose transporters within MS; the effects of polyphenols as anti-oxidant, anti-inflammatory and anti-angiogenic compounds. The role of NFkB, nitric oxide synthases, hypoxia-inducible factors, and many other molecules that play a part in the development of oxidative stress and inflammation as well as angiogenesis is also covered. This book fills the gap between basic science and medical care, and provides the reader with the skills to apply rigorous basic science to clinical settings of metabolic syndrome-associated disorders.
Book Synopsis Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome by : Raquel Soares
Download or read book Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome written by Raquel Soares and published by Springer Science & Business Media. This book was released on 2009-02-25 with total page 213 pages. Available in PDF, EPUB and Kindle. Book excerpt: Metabolic Syndrome (MS) is a highly prevalent condition in developed countries and is a cluster of several risk factors for type 2 diabetes and cardiovascular disease that includes increased body mass index/waist circumference, visceral obesity, insulin resistance, hyperclycaemia, dyslipidaemia and hypertension, which are all major causes of morbidity and death. This volume provides a critical review and discussion of the knowledge gathered on MS and analyzes the interplay between oxidative stress, chronic inflammation and angiogenesis features. There is a special focus on recent discoveries and progress toward possible therapeutic strategies, such as the role of glucose transporters within MS; the effects of polyphenols as anti-oxidant, anti-inflammatory and anti-angiogenic compounds. The role of NFkB, nitric oxide synthases, hypoxia-inducible factors, and many other molecules that play a part in the development of oxidative stress and inflammation as well as angiogenesis is also covered. This book fills the gap between basic science and medical care, and provides the reader with the skills to apply rigorous basic science to clinical settings of metabolic syndrome-associated disorders.
Pathologic angiogenesis is involved in cancer and several blinding conditions such as wet age-related macular degeneration, proliferative retinopathies and corneal neovascularization. In these dieseases, the angiogenic triggers are hypoxia and inflammation, and both involve the main angiogenic mediator, which is Vascular Endothelial Growth Factor (VEGF). Among available treatments, anti-VEGF often shows limited or temporary efficacy, while steroids are potentially responsible for many side-effects. This thesis presents a series of linked studies aimed at elucidating the early pathologic changes leading to inflammation and corneal neovascularization, and how various treatments affect this process. In this thesis, anti-inflammatory and anti-angiogenic treatments are applied in corneal neovascularization models, to identify VEGF-independent pathways and other novel factors as future therapy targets, as well as to investigate the endogenous modulation of angiogenesis. A model of experimental neovascularization in the rat cornea was used as main model, where the neovascular response is triggered by a surgical suture placed into the cornea. Investigational treatments (anti-Vegf, dexamethasone, IMD0354, Gap27, or control substances) were then given topically, with the exception of IMD0354, which was given systemically. The effects in the cornea were studied in vivo with slit lamp photography to assess and quantify macroscopic vessel growth and using in vivo confocal microscopy (IVCM) to study cell infiltration and limbal vessel dilation and detect microscopic vessel sprouts; these examinations were performed longitudinally. Genomic analysis with RNA microarray, selected gene expression with q-RT-PCR, and selected protein expression in tissue (immunohistochemistry, immunofluorescence, Western blot) were performed at different time-points. Moreover, other experiments on cell cultures (HUVEC and HCEC), organ cultures (human corneas), ex vivo models (aortic rings) and in vivo studies (zebrafish vasculogenesis) were performed. Dexamethasone suppressed limbal vasodilation and corneal neovascularization more than anti-Vegf, despite no difference in inflammatory cell infiltration into the cornea. Five-hundred eleven fewer genes were differentially expressed in dexamethasone-treated corneas relative to naïve corneas, compared to anti-Vegf. Among them, several major pro-angiogenic and pro-inflammatory factors and chemokines were suppressed only by dexamethasone and represent novel candidate factors to target in order to improve anti-VEGF treatment. On the other hand, selective inhibition of a single inflammatory pathway (NF-?B), despite showing similar early effects as dexamethasone in suppressing tissue inflammation, was not effective enough to suppress new vessel growth. The same factors suppressed by dexamethasone are also inhibited in endogenous modulation of angiogenesis. Surprisingly, dexamethasone activated several complement factors, which could possibly be beneficial in the anti-angiogenic response. In a different therapeutic approach, promoting cell migration to accelerate epithelial wound closure similarly was not sufficient to avoid inflammation and angiogenesis in the cornea. In conclusion, new and more effective treatments are needed for corneal inflammation and neovascularization with fewer side-effects. In this thesis, several novel factors and mechanisms related to inflammation are identified, factors that are not addressed by anti-Vegf therapy, and therefore represent interesting objects for further study, as they have the potential to be targets for adjuvant therapy. Specific anti-inflammatory treatment as well as therapeutic activation of endogenous regulatory pathways, and potentially complement modulation, might represent new strategies to improve anti-angiogenic therapy, but when used alone they do not seem to avoid corneal neovascularization.
Book Synopsis Inhibitors of corneal inflammation and angiogenesis by : Pierfrancesco Mirabelli
Download or read book Inhibitors of corneal inflammation and angiogenesis written by Pierfrancesco Mirabelli and published by Linköping University Electronic Press. This book was released on 2019-04-30 with total page 91 pages. Available in PDF, EPUB and Kindle. Book excerpt: Pathologic angiogenesis is involved in cancer and several blinding conditions such as wet age-related macular degeneration, proliferative retinopathies and corneal neovascularization. In these dieseases, the angiogenic triggers are hypoxia and inflammation, and both involve the main angiogenic mediator, which is Vascular Endothelial Growth Factor (VEGF). Among available treatments, anti-VEGF often shows limited or temporary efficacy, while steroids are potentially responsible for many side-effects. This thesis presents a series of linked studies aimed at elucidating the early pathologic changes leading to inflammation and corneal neovascularization, and how various treatments affect this process. In this thesis, anti-inflammatory and anti-angiogenic treatments are applied in corneal neovascularization models, to identify VEGF-independent pathways and other novel factors as future therapy targets, as well as to investigate the endogenous modulation of angiogenesis. A model of experimental neovascularization in the rat cornea was used as main model, where the neovascular response is triggered by a surgical suture placed into the cornea. Investigational treatments (anti-Vegf, dexamethasone, IMD0354, Gap27, or control substances) were then given topically, with the exception of IMD0354, which was given systemically. The effects in the cornea were studied in vivo with slit lamp photography to assess and quantify macroscopic vessel growth and using in vivo confocal microscopy (IVCM) to study cell infiltration and limbal vessel dilation and detect microscopic vessel sprouts; these examinations were performed longitudinally. Genomic analysis with RNA microarray, selected gene expression with q-RT-PCR, and selected protein expression in tissue (immunohistochemistry, immunofluorescence, Western blot) were performed at different time-points. Moreover, other experiments on cell cultures (HUVEC and HCEC), organ cultures (human corneas), ex vivo models (aortic rings) and in vivo studies (zebrafish vasculogenesis) were performed. Dexamethasone suppressed limbal vasodilation and corneal neovascularization more than anti-Vegf, despite no difference in inflammatory cell infiltration into the cornea. Five-hundred eleven fewer genes were differentially expressed in dexamethasone-treated corneas relative to naïve corneas, compared to anti-Vegf. Among them, several major pro-angiogenic and pro-inflammatory factors and chemokines were suppressed only by dexamethasone and represent novel candidate factors to target in order to improve anti-VEGF treatment. On the other hand, selective inhibition of a single inflammatory pathway (NF-?B), despite showing similar early effects as dexamethasone in suppressing tissue inflammation, was not effective enough to suppress new vessel growth. The same factors suppressed by dexamethasone are also inhibited in endogenous modulation of angiogenesis. Surprisingly, dexamethasone activated several complement factors, which could possibly be beneficial in the anti-angiogenic response. In a different therapeutic approach, promoting cell migration to accelerate epithelial wound closure similarly was not sufficient to avoid inflammation and angiogenesis in the cornea. In conclusion, new and more effective treatments are needed for corneal inflammation and neovascularization with fewer side-effects. In this thesis, several novel factors and mechanisms related to inflammation are identified, factors that are not addressed by anti-Vegf therapy, and therefore represent interesting objects for further study, as they have the potential to be targets for adjuvant therapy. Specific anti-inflammatory treatment as well as therapeutic activation of endogenous regulatory pathways, and potentially complement modulation, might represent new strategies to improve anti-angiogenic therapy, but when used alone they do not seem to avoid corneal neovascularization.
This much-needed text develops current knowledge on the mechanisms of angiogenesis at the molecular and cellular levels as they relate to inflammation, including acute and chronic inflammation, neurogenic initiation, and the role of the multiple cellular components that comprise inflammation. The volume brings together experts in each of these fields to link the molecular and cellular processes in angiogenesis to those of inflammation and disease, culminating in a discourse on areas for future therapies.
Book Synopsis Angiogenesis in Inflammation: Mechanisms and Clinical Correlates by : Michael Seed
Download or read book Angiogenesis in Inflammation: Mechanisms and Clinical Correlates written by Michael Seed and published by Birkhäuser. This book was released on 2009-08-29 with total page 180 pages. Available in PDF, EPUB and Kindle. Book excerpt: This much-needed text develops current knowledge on the mechanisms of angiogenesis at the molecular and cellular levels as they relate to inflammation, including acute and chronic inflammation, neurogenic initiation, and the role of the multiple cellular components that comprise inflammation. The volume brings together experts in each of these fields to link the molecular and cellular processes in angiogenesis to those of inflammation and disease, culminating in a discourse on areas for future therapies.
Dr. Judah Folkman is considered the "father of angiogenesis." Because of Folkman's discovery and research, the possibilities of angiogenic therapy have broadened beyond cancer to many noncancerous diseases. Angiogenesis: An Integrative Approach from Science to Medicine is a comprehensive, concise summary of tumor angiogenesis. It is an up-to-date and authoritative reference for the angiogenesis field as it relates to oncology. This book represents the first collection in a volume of which Folkman is co-editor. Folkman has authored nearly 400 original papers and more than 100 book chapters.
Book Synopsis Angiogenesis by : William D. Figg
Download or read book Angiogenesis written by William D. Figg and published by Springer Science & Business Media. This book was released on 2008-05-24 with total page 592 pages. Available in PDF, EPUB and Kindle. Book excerpt: Dr. Judah Folkman is considered the "father of angiogenesis." Because of Folkman's discovery and research, the possibilities of angiogenic therapy have broadened beyond cancer to many noncancerous diseases. Angiogenesis: An Integrative Approach from Science to Medicine is a comprehensive, concise summary of tumor angiogenesis. It is an up-to-date and authoritative reference for the angiogenesis field as it relates to oncology. This book represents the first collection in a volume of which Folkman is co-editor. Folkman has authored nearly 400 original papers and more than 100 book chapters.
Targeting Angiogenesis, Inflammation and Oxidative Stress in Chronic Diseases presents recent advances in the vivid molecular pathways targeting angiogenesis, inflammation and oxidative stress that contribute very widely to the genesis of chronic diseases. The books will also highlight the drugs from natural and synthetic origin in the management/prevention/treatment of diseases along with the drug delivery approaches. The book’s authors from various key institutions around the globe will deliver well-structured and well-designed chapters. The systematic presented information and knowledge will surely aid consistency and continuity. The multifaceted book is enriched with deep scientific contents. Each chapter will clearly define the facts, emerging role of molecular pathways and the targets and focus will be imparted on key challenges associated and the future directions that will provide torch bearer thing for the researchers to explore new targets in the domain. Focuses on the pathogenesis of the disease, along with the molecular mechanism of action Includes updates on strategic design/delivery of drugs targeting angiogenesis, inflammation, and oxidative stress Provides recent advancements in the field of pathogenesis of chronic diseases
Book Synopsis Targeting Angiogenesis, Inflammation and Oxidative Stress in Chronic Diseases by : Tapan Behl
Download or read book Targeting Angiogenesis, Inflammation and Oxidative Stress in Chronic Diseases written by Tapan Behl and published by Elsevier. This book was released on 2024-01-26 with total page 524 pages. Available in PDF, EPUB and Kindle. Book excerpt: Targeting Angiogenesis, Inflammation and Oxidative Stress in Chronic Diseases presents recent advances in the vivid molecular pathways targeting angiogenesis, inflammation and oxidative stress that contribute very widely to the genesis of chronic diseases. The books will also highlight the drugs from natural and synthetic origin in the management/prevention/treatment of diseases along with the drug delivery approaches. The book’s authors from various key institutions around the globe will deliver well-structured and well-designed chapters. The systematic presented information and knowledge will surely aid consistency and continuity. The multifaceted book is enriched with deep scientific contents. Each chapter will clearly define the facts, emerging role of molecular pathways and the targets and focus will be imparted on key challenges associated and the future directions that will provide torch bearer thing for the researchers to explore new targets in the domain. Focuses on the pathogenesis of the disease, along with the molecular mechanism of action Includes updates on strategic design/delivery of drugs targeting angiogenesis, inflammation, and oxidative stress Provides recent advancements in the field of pathogenesis of chronic diseases
Endothelial cells form the inner lining of blood and lymphatic vessels and they have frequent interactions with immune cells as well as foreign agents. Endothelial function is crucially involved in physiologic immunity at different stages including recruitment of leukocytes, angiogenesis and tissue repair. Endothelial dysfunction is a not well-defined term, it is widely used to describe the non-physiologic activity of endothelial cells. It has been suggested that endothelial dysfunction plays a role in a variety of human diseases, such as arteriosclerosis, cancer, autoimmunity and sepsis. More recently, a role of lymphatic endothelial cells as well as vascular endothelial cells in the pathophysiology of inflammation and allo-immune reactions has been suggested. Development of novel therapeutic approaches to normalize endothelial dysfunction is currently an unmet medical need. Until now, the cellular and molecular mechanisms of mutual influences between endothelial dysfunction and human diseases remain largely unexplored, constituting a frontier hindering the development of new therapies. This Research Topic aims to build a forum for a wide range of scientific studies in the fields of endothelial dysfunction during inflammatory diseases and transplantation.
Book Synopsis Endothelial Dysfunction During Inflammation and Alloimmunity by : Olaf Penack
Download or read book Endothelial Dysfunction During Inflammation and Alloimmunity written by Olaf Penack and published by Frontiers Media SA. This book was released on 2019-04-09 with total page 126 pages. Available in PDF, EPUB and Kindle. Book excerpt: Endothelial cells form the inner lining of blood and lymphatic vessels and they have frequent interactions with immune cells as well as foreign agents. Endothelial function is crucially involved in physiologic immunity at different stages including recruitment of leukocytes, angiogenesis and tissue repair. Endothelial dysfunction is a not well-defined term, it is widely used to describe the non-physiologic activity of endothelial cells. It has been suggested that endothelial dysfunction plays a role in a variety of human diseases, such as arteriosclerosis, cancer, autoimmunity and sepsis. More recently, a role of lymphatic endothelial cells as well as vascular endothelial cells in the pathophysiology of inflammation and allo-immune reactions has been suggested. Development of novel therapeutic approaches to normalize endothelial dysfunction is currently an unmet medical need. Until now, the cellular and molecular mechanisms of mutual influences between endothelial dysfunction and human diseases remain largely unexplored, constituting a frontier hindering the development of new therapies. This Research Topic aims to build a forum for a wide range of scientific studies in the fields of endothelial dysfunction during inflammatory diseases and transplantation.
