Fibroblast Growth Factor 23, 1st Edition, by Elsevier
Fibroblast Growth Factor 23 describes how FGF23 was initially identified as a bone-derived factor targeting the kidney. As such, sections in this comprehensive book cover exciting research that shows that different FGF23 effects require distinct signaling receptors and mediators that differ among target tissues, cover FGF23 initially identified as a bone-derived factor targeting the kidney, look at FGF23 as a regulator of phosphate metabolism and beyond, and cover research on novel concepts of FGF receptor signaling. Additional sections cover biochemistry, pharmacology, and nephrology, making this book an ideal reference source on FGF23.
Chapter accepted by Editors: Dr. Faul gave it a “green light” and moved the process to the printing and formating.
Dr. C. Faul from the University of Alabama is one of the “fashion setters” toward a better understanding of FGFs in Nephro and Cardiovascular Systems.
This project was an incredible opportunity for personal and professional growth. I was very fortunate to work on one chapter for this book, where Dr. Razzaque smoothly guided us through the process and Editors’ communication.
This Book is currently on Pre-Order 🙂
- Provides a comprehensive collection of chapters on the diversity of FGF23’s actions
- Highlights truly translational topics, from molecular signaling to physiology and mechanism of disease, discussing cell culture and animal models to study FGF23
- Describes FGF23’s potential in the clinical setting as a biomarker or even drug target
- Presents leaders in the field who cover a wide spectrum of research backgrounds and expertise, including clinical and basic scientists who specialize in diseases, endocrinology, genetics, protein biochemistry, cell biology, and physiology
Biomedical researchers and research clinicians in the field researching FGF23; basic scientists in physiology, biochemistry, and genetics, clinicians such as nephrologists, bone, and mineral researchers and endocrinologists
Table of Contents
1. The discovery of FGF23 – a historic view: genetic disorders of hypo- and hyperphosphatemia
Michael J. Econs
2. FGF23 – an established master regulator of phosphate metabolism
3. FGF23 – more than a phosphaturic hormone
Reinhold G. Erben
4. The regulation of FGF23 production in bone and outside of bone
5. Klotho-dependent actions of FGF23 – targets, signal transduction and cellular effects
6. Klotho-independent actions of FGF23 – targets, signal transduction and cellular effects
7. The experimental detection of FGF23 responsiveness and effects
8. FGF23 and bone disease
Katherine Wesseling Perry
9. FGF23 and kidney disease
10. FGF23 and heart and vascular disease
11. FGF23 and inflammation, anemia, and iron
Mark R. Hanudel
12. FGF23 and infectious diseases
13. FGF23 and lung disease
14. FGF23 and neuro-cognitive disorders
15. FGF23 measurements in humans and its place as a clinical biomarker
Edward R. Smith
16. FGF23 – a drug target including treatment of hypophosphatemic osteomalacia
17. FGF23 – resolved issues, remaining controversies and future questions – a clinician’s perspective
Gunnar Henrik Heine
18. Klotho – the discovery of the FGF23 co-receptor
19. Klotho – an FGF23-independent hormone
20. Klotho and aging phenotypes
21. αKlotho gene and protein measurements in humans and their role as a clinical biomarker of disease
22. Structural Basis of FGF23 Hormone Signaling
23. Klotho – open questions, controversies and future perspectives
24. The crosstalk between phosphate, FGF23 and klotho in the regulation of tissue homeostasis in health and disease
Erem S., He, P., Razzaque, M.S
Decreased bone mass and an increased risk of bone fractures become more common with age. This condition is often associated with osteoporosis and is caused by an imbalance of bone resorption and new bone formation. Lifestyle factors that affect the risk of osteoporosis include alcohol, diet, hormones, physical activity, and smoking. Calcium and vitamin D are particularly important for the age-related loss of bone density and skeletal muscle mass, but other minerals, such as magnesium, also have an important role. Here, we summarize how optimal magnesium and vitamin D balance improve health outcomes in the elderly, the role of magnesium and vitamin D on bone formation, and the implications of widespread deficiency of these factors in the United States and worldwide, particularly in the elderly population.
Phosphate is a common ingredient in many healthy foods but, it is also present in foods containing additives and preservatives. When found in foods, phosphate is absorbed in the intestines and filtered from the blood by the kidneys. Generally, any excess is excreted in the urine. In renal pathologies, however, such as chronic kidney disease, a reduced renal ability to excrete phosphate can result in excess accumulation in the body. This accumulation can be a catalyst for widespread damage to the cellular components, bones, and cardiovascular structures. This in turn can reduce mortality. Because of an incomplete understanding of the mechanism for phosphate homeostasis, and the multiple organ systems that can modulate it, treatment strategies designed to minimize phosphate burden are limited.
We all know that too much exposure to UV radiation from the sun can cause skin cancer. It is equally well known that the production of Vitamin D as a result of sunlight exposure has many benefits, not the least of which is its positive impact on bone health and conditions such as rickets, osteoporosis, and osteomalacia, to name a few. What is not well known is the benefits of sunlight exposure beyond Vitamin D production. Our review suggests that sunlight exposure, independent of vitamin D, has positive/moderating effects on colorectal cancer, diabetes, hypertension, immune-mediated inflammatory diseases, multiple sclerosis, and obesity. Covid-19 and its relationship to sunlight exposure and vitamin D are also reviewed.