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For the past 100 years the mainstay of therapy for rheumatoid arthritis (RA) has been aspirin or other drugs of the non-steroid anti-inflammatory group. In 1971 Vane pro posed that both the beneficial and toxic actions of these drugs was through inhibition of prostaglandin synthesis. The recent discovery that prostaglandins responsible for pain and other symptoms at inflammatory foci are synthesized by an inducible cyclooxygenase (COX-2) that is encoded by a gene distinct from that of the consti tutive enzyme (COX-I) provided a new target for therapy of RA. A drug that would selectively inhibit COX-2 would hopefully produce the symptomatic benefit provided by existing NSAIDs without the gastrointestinal and renal toxicity due to the inhibition of COX-I. Drugs selective for COX-2 are now available. Experimental studies have shown them to be effective with minimal toxicity, and in clinical trials gastric and renal toxicities are less. Highly selective COX-2 inhibitors, perhaps designed with knowledge of the crystal structures of COX-I and COX-2, are also available. Other experimental studies, including those in animals lacking effective genes for COX-lor COX-2 and in experimental carcinomas, suggest there is still much to be learned of the pathophysiological functions of these enzymes. The inflammatory response is a complex reaction involving many mediators that derive from white blood cells, endothelial cells and other tissues. Preliminary data have revealed that inhibitors of the cytokines and adhesion molecules that play a crucial role in the migration of white cells to inflammatory sites may be useful in RA.
Inflammation has been described as the basis of many pathologies of human disease. When one considers the updated signs of inflammation, they would be vasodilation, cell migration, and, in the case of chronic inflam- tion, cell proliferation, often with an underlying autoimmune basis. Gen- ally, inflammation may be divided into acute, chronic, and autoimmune, - though the editors believe that most, if not all, chronic states are often the result of an autoimmune response to an endogenous antigen. Thus, a proper understanding of the inflammatory basis may provide clues to new therap- tic targets not only in classical inflammatory diseases, but atherosclerosis, cancer, and ischemic heart disease as well. The lack of advances in classical inflammatory diseases, such as rh- matoid arthritis, may in part arise from a failure to classify the disease into different forms. That different forms exist is exemplified in patients with d- fering responses to existing antiinflammatory drugs, ranging from nonresponders to very positive responders for a particular nonsteroidal an- inflammatory drug (NSAID). Though researchers have progressively unr- eled the mechanisms, the story is far from complete. It should also be noted that the inflammatory response is part of the innate immune response, or to use John Hunter’s words in 1795, “inflammation is a salutary response.” That may be applied in particular to the defensive response to invading micro- ganisms.
The study of inflammation has captured the interest of scholars since the earliest recorded history. Symbols identifying the cardinal signs of inflammation were uncovered in both Sanskrit and hieroglyphics (1). Since complete apprecia tion of the inflammatory process is underscored by the need for knowledge at both the cellular and molecular levels, academic inquiry in the area of inflammation has led, in many respects, the foray of current biomedical research. Molecular and Cellular Basis of Inflammation represents research from the cutting edge in the broad view of inflammation. The chapters are written by experts with a multidisciplinary approach to the study of inflammatory and cellular processes, and thus include contributions form the fields of molecular biology, biochemistry, pharmacology, immunology, and pathobiology. Molecular and Cellular Basis of Inflammation was first conceived during a mini symposium sponsored by the American Society for Investigative Pathology held at FASEB in 1995 entitled "The Role of Reactive Lipids, Oxygen and Nitro gen Metabolites in Inflammation," at which several of the contributing authors delivered lectures. This present, much-extended volume includes leading-front descriptions of both protein and lipid mediators. The chapter devoted to the comple ment cascade by Ward and colleagues, as well as Chapters 3-7 and 13, provide up to-date descriptions of the biosynthesis, molecular biology, chemistry, and actions of both protein and lipid mediators.
Non-communicable diseases (NCDs) are chronic diseases that include most ageing-related diseases, representing the main cause of death and disability in the general population. Inflammation and oxidative stress are common features in NCDs, responsible for the cell, tissue, and organ damage that contributes to the progression of these diseases. They may be also key targets for the development of novel preventive and therapeutic strategies. This Special Issue includes 14 peer-reviewed papers, including 12 original research papers and 2 reviews. Together, they represent the most recent progress in the field of several degenerative disorders, aiming to establish specific biomarkers, detailing the pathogenesis and the evolution of these diseases, making a correct diagnosis, and opening up new therapeutic strategies. Of relevance, many studies report the beneficial effects of natural compounds, derived from several plants, leaves, and fruits; their antioxidant and anti-inflammatory properties suggest their use as a dietary supplement for prevention and/or complement to standard therapies.
This book, now in a thoroughly revised and updated second edition, provides the latest information on cancer metastasis from the perspective of inflammation and presents new ideas on the complicated mechanisms of metastasis and potential therapeutic targets. Key features include discussion of mechanisms recently identified to be involved in the resolution phase of inflammation, presentation of the latest evidence regarding the roles of endogenous TLR4 ligands in metastasis, and thorough explanation of the concept of homeostatic inflammation and current understanding of the significance of its dysregulation for metastasis. Structure-based thinking is another important element of the book, and it is proposed that inflammation forms a functional triangle with angiogenesis and coagulation, at the center of which cancer is located. Examples of the many additional specific topics covered in this edition include the functional involvement of new types of RNA in cancer, the insights offered by recent advances in bioinformatics, and the potential of a casein kinase 1α inhibitor in the treatment of acute myeloid leukemia. The book will be a valuable update and resource for both experienced and younger researchers. Homeostasis, originated from an idea of internal milieu by Claude Bernard, is eventually maintained by endogenous elements. The essential features of inflammation are leukocyte mobilization and increased vascular permeability, which could take place in many homeostatic or physiological conditions at low levels. Homeostatic inflammation is a concept to explain pathological settings such as metastasis in which irrespective of its level those inflammatory features are misused with endogenous molecules (see Chap. 14,15). As inflammation comprises many biological fields, targeting a single molecule for a disease could potentially make a therapeutic contribution to other diseases. For example, one focus is applied here to the roles of calprotectin in lung metastasis, which is implicated in psychiatric disorders and COVID-19 as shown by recent evidence.
This volume focuses on therapeutic targets that were identified after TNF blockade. All these targets have recently been registered or are currently under development for the treatment of rheumatoid arthritis. Each chapter explores the biological rationale of a distinct therapeutic target in great detail. Readers will discover the latest in vitro work, animal models, and results from clinical trials.
Anti-Inflammatory Drug Discovery provides a comprehensive review of recent medicinal chemistry approaches to a variety of important therapeutic targets and provides a key reference for those interested in the prosecution of modern drug discovery programs directed at anti-inflammatory mechanisms of action. The editors, with extensive experience in this field, have selected key thought-leaders who will bring their experience to the medicinal chemistry literature for each target, ranging from components of the arachadonic acid cascade, to kinases, GPCRs, sphingolipids and others, to summarize its background biology and detail new insights, major advances and issues related to bringing new anti-inflammatory therapies to market. Consisting of five main sections key targets covered will include the AA Cascade: mPGES1, cPLA2, Leukotriene A4 Hydrolase, CRTH2; Kinases: P38/PDE4, MAPKAP Kinase 2 (MK2), Syk Kinase Inhibitors, Jak Kinases, IKK , Bruton's Tyrosine Kinase; GPCRs: CCR1, CCR2 Antagonists, CB2 Agonists; Sphingolipids: S1P1 Receptor Agonists, Sphingosine Lyase and Sphingosine Kinase 1 and a final miscellaneous section that looks at Non-Steroidal Dissociated Glucocorticoid Receptor Agonists. The book will be essential reading for pharmacologists, medicinal chemists and pharmaceutical scientists working in industry and academia.