Cellular Stress Regulates Fibroblast Growth Factor 23 Fgf23 And Klotho

Fibroblast Growth Factor 23 describes how FGF23 was initially identified as a bone-derived factor targeting the kidney. This reference then defines the exciting research in recent years how a much wider spectrum of sources, targets and functions have been identified, showing that different FGF23 effects require distinct signaling receptors and mediators that differ among target tissues. This reference reaches a wide academic audience with a broad interest in biomedical sciences, including: Endocrinology: FGF23 initially identified as a bone-derived factor targeting the kidney Physiology: FGF23 as a regulator of phosphate metabolism and beyond Cell Biology: Mechanistic FGF23 research revealed novel concepts of FGF receptor signaling Biochemistry: Molecular crosstalk between FGF23 and klotho, from structure and binding to signal transduction Pharmacology: FGF23 and its receptors as potential drug targets to treat or prevent diseases, such as CKD, heart failure or COPD Basic Research: Cell culture and animal models as well as novel assays to study FGF23 production and effects Nephrology: FGF23 as a biomarker and cause for CKD and associated pathologies Internal Medicine: FGF23 as a biomarker and cause for various diseases involving the kidney, heart, lung and liver

Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various metabolic processes in adulthood. Such FGFs, collectively called endocrine FGFs, are comprised of three members (FGF15/19, FGF21, and FGF23: FGF15 is the mouse ortholog of human FGF19). These endocrine FGFs share a common structural feature that enables the endocrine mode of action at the expense of the affinity to FGF receptors. To restore the affinity to FGF receptors in their target organs, the endocrine FGFs have designated the Klotho family of transmembrane proteins as obligate co-receptors. By expressing Klothos in a tissue-specific manner, this unique co-receptor system also enables the endocrine FGFs to specify their target organs among many tissues that express FGF receptors.

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Written by world experts, this books follows upon the monumental success of the first edition of The Parathyroids, which was universally acclaimed as the best text on the subject. An authoritative reference that spans the basic science of parathyroid hormone treatment to major clinical disorders in a superb, single compendium, The Parathyroids offers an objective and authoritative view on controversial clinical issues in this rapidly changing field. Every medical school library and virtually every major hospital library will need this book as a reference for students and clinicians. Key Features * Offers objective and authoritative reviews on controversial clinical issues * Written by world experts on parathyroid hormone and its disorders * Superb, state-of-the-art compendium in one convenient volume * Bridges basic science of parathyroid hormone to major clinical disorders * Practical information on clinical management of parathyroid hormone disorders

EDITOR-IN-CHIEF: Clifford J. Rosen, M.D., Maine Medical Center Research Institute, Scarborough, Maine SENIOR ASSOCIATE EDITORS: Juliet E. Compston, M.D., FRCP, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom Jane B. Lian, Ph.D., University of Massachusetts Medical School, Worcester, Massachusetts This comprehensive yet concise handbook is an indispensable reference for the many clinicians who see patients with disorders of bone formation, metabolic bone diseases, or disorders of stone formation. It is also a crucial tool for researchers, students, and all other professionals working in the bone field. In a format designed for quick reference, it provides complete information on the symptoms, pathophysiology, diagnosis, and treatment of all common and rare bone and mineral disorders. New in this edition: detailed coverage of osteonecrosis of the jaw, more in-depth coverage of cancer and bone including new approaches to pathogenesis, diagnosis, and treatment; new approaches to anabolic therapy of osteoporosis; the latest research on Vitamin D; expanded coverage of international topics; more on the genetics of bone mass; and newer imaging techniques for the skeleton. In addition, this edition features a free, online-only appendix of medicines used to treat bone disorders and their availability around the world.

The enormous progress made during the last decade has resulted in a better conceptual understanding of mineral ion metabolism in general. With regard to chronic kidney disease, the two most affected nutrients are phosphate and vitamin D. This book provides an overview of the physiological aspects of phosphate and vitamin D metabolism, and how their pathological dysregulation facilitates advancement of chronic kidney disease. It looks into the complex molecular and organ cross-talks during disease progression that range from the involvement of fibroblast growth factor (FGF23)-klotho system to impaired phosphate transport to hormonal dysfunctions of PTH and vitamin D. Each chapter clearly presents the clinically and biologically important problems and lists the key unsolved issues related to chronic kidney disease and beyond. Illustrations explaining multi-factorial and multi-organ interactions provide an easy outline for the reader to appreciate the complex biological pathways. For those without prior familiarity with the subject matter, this volume may serve as a quick reference to get updated information on phosphate and vitamin D metabolism.

Known worldwide, chronic kidney disease (CKD) is a disease that affects up to 4% of the population with increasing figures also in the developing countries. Life expectancy of patients affected by CKD is shortened compared to the overall population, and only a minority of patients reach end-stage renal disease (ESRD) with the need for dialysis or renal transplantation; death overtakes dialysis. In the 13 chapters, this book sheds light on the different aspects related to pathophysiology and clinical aspects of CKD, providing interesting insights into not only inflammation and cardiovascular risk but also the interplay of hormones and the functional aspects of endothelial function. In addition, chapters dealing with genetic aspects of polycystic kidney disease and also the clinical handling of patients with CKD and peritoneal dialysis will be beneficial for the open-minded reader.