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Phosphate-Related Disorders: From Physiology to Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 12336

Special Issue Editors


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Guest Editor
Endocrinology and Metabolism Unit, University Hospital Udine, 33100 Udine, Italy
Interests: osteoporosis; metabolic bone diseases; renal stone disease and mineral metabolism disorders, parathyroid diseases; thyroid diseases
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Co-Guest Editor
Unit of Endocrinology and Diabetes, Campus Bio-Medico University, 00128 Rome, Italy
Interests: PTH; hyperparathyroidism; hypoparathyroidism; calcium; phosphate; thyroid; diabetes
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E-Mail Website
Co-Guest Editor
Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
Interests: osteoporosis; metabolic bone diseases; Paget’s disease of bone; type 2 diabetes
Special Issues, Collections and Topics in MDPI journals

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Co-Guest Editor
Unit of Endocrinology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy
Interests: osteoporosis; metabolic bone diseases; parathyroid diseases; multiple endocrine neoplasia; genetic diseases of bone
Special Issues, Collections and Topics in MDPI journals

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Co-Guest Editor
1. Department of Medical Biotechnology and Translational Medicine, University of Milan, 20122 Milan, Italy
2. Unit of Endocrinology, ASST Ospedale Niguarda, 20162 Milan, Italy
Interests: adrenal diseases; parathyroid diseases; osteoporosis; metabolic bone diseases; endocrine hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Phosphorus is essential for many fundamental functions in the human body, where it is present mainly as the anion phosphate (PO43–) that forms a variety of different salts, among which skeletal hydroxyapatite is the most abundant.

Phosphate is also a key structural element of DNA, adenosine triphosphate (ATP), and cell membranes and is involved in several enzymatic reactions and protein functions.

Due to its importance, phosphate homeostasis is strictly controlled by parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) through their actions on the kidney, intestine, and bone. Physicians frequently evaluate the so-called calcium/phosphate metabolism, but their main interest is usually focused on calcium, leaving the role of the “Cinderella-ion” to phosphate. Actually, since the discovery of FGF-23 in 2000, a higher attention has been paid to phosphate metabolism, and many phosphate-associated diseases have been discovered or rediscovered.

This Special Issue aims to present recent advances in the understanding of phosphate handling in the human body. We invite investigators to contribute original research articles and reviews on pathophysiologic processes, diagnosis, and treatments of phosphate-related disorders.

Dr. Fabio Vescini
Dr. Andrea Palermo
Prof. Dr. Luigi Gennari
Dr. Alberto Falchetti
Prof. Dr. Iacopo Chiodini
Guest Editors

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Keywords

  • Hypophosphatemia
  • Hypophosphatemia
  • Metabolic Bone Disease
  • Tumor Induced Osteomalacia
  • Rickets
  • Genetics
  • Renal Stone Disease
  • Chronic Kidney Disease
  • Iron Disorders
  • Endocrine Diseases
  • Drug-Induced Hypophosphatemia

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Published Papers (3 papers)

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Review

17 pages, 1039 KiB  
Review
Phosphate in the Context of Cognitive Impairment and Other Neurological Disorders Occurrence in Chronic Kidney Disease
by Merita Rroji, Andreja Figurek, Davide Viggiano, Giovambattista Capasso and Goce Spasovski
Int. J. Mol. Sci. 2022, 23(13), 7362; https://doi.org/10.3390/ijms23137362 - 1 Jul 2022
Cited by 10 | Viewed by 3335
Abstract
The nervous system and the kidneys are linked under physiological states to maintain normal body homeostasis. In chronic kidney disease (CKD), damaged kidneys can impair the central nervous system, including cerebrovascular disease and cognitive impairment (CI). Recently, kidney disease has been proposed as [...] Read more.
The nervous system and the kidneys are linked under physiological states to maintain normal body homeostasis. In chronic kidney disease (CKD), damaged kidneys can impair the central nervous system, including cerebrovascular disease and cognitive impairment (CI). Recently, kidney disease has been proposed as a new modifiable risk factor for dementia. It is reported that uremic toxins may have direct neurotoxic (astrocyte activation and neuronal death) and/or indirect action through vascular effects (cerebral endothelial dysfunction, calcification, and inflammation). This review summarizes the evidence from research investigating the pathophysiological effects of phosphate toxicity in the nervous system, raising the question of whether the control of hyperphosphatemia in CKD would lower patients’ risk of developing cognitive impairment and dementia. Full article
(This article belongs to the Special Issue Phosphate-Related Disorders: From Physiology to Diseases)
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12 pages, 868 KiB  
Review
Phosphate Metabolism and Pathophysiology in Parathyroid Disorders and Endocrine Tumors
by Guido Zavatta, Paola Altieri, Giulia Vandi, Valentina Vicennati, Uberto Pagotto and Fabio Vescini
Int. J. Mol. Sci. 2021, 22(23), 12975; https://doi.org/10.3390/ijms222312975 - 30 Nov 2021
Cited by 4 | Viewed by 5099
Abstract
The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, and also of rarer endocrine metabolic bone diseases, such as hypoparathyroidism and tumor-induced hypophosphatemia. These rare diseases of mineral metabolism [...] Read more.
The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, and also of rarer endocrine metabolic bone diseases, such as hypoparathyroidism and tumor-induced hypophosphatemia. These rare diseases of mineral metabolism have been and will be a precious source of new information about phosphate and other minerals in the coming years. The parathyroid glands, the kidneys, and the intestine are the main organs affecting phosphate levels in the blood and urine. Parathyroid disorders, renal tubule defects, or phosphatonin-producing tumors might be unveiled from alterations of such a simple and inexpensive mineral as serum phosphate. This review will present all these disorders from a ‘phosphate perspective’. Full article
(This article belongs to the Special Issue Phosphate-Related Disorders: From Physiology to Diseases)
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16 pages, 1746 KiB  
Review
Extracellular Inorganic Phosphate-Induced Release of Reactive Oxygen Species: Roles in Physiological Processes and Disease Development
by Marco Antonio Lacerda-Abreu and José Roberto Meyer-Fernandes
Int. J. Mol. Sci. 2021, 22(15), 7768; https://doi.org/10.3390/ijms22157768 - 21 Jul 2021
Cited by 15 | Viewed by 3085
Abstract
Inorganic phosphate (Pi) is an essential nutrient for living organisms and is maintained in equilibrium in the range of 0.8–1.4 mM Pi. Pi is a source of organic constituents for DNA, RNA, and phospholipids and is essential for ATP formation mainly through energy [...] Read more.
Inorganic phosphate (Pi) is an essential nutrient for living organisms and is maintained in equilibrium in the range of 0.8–1.4 mM Pi. Pi is a source of organic constituents for DNA, RNA, and phospholipids and is essential for ATP formation mainly through energy metabolism or cellular signalling modulators. In mitochondria isolated from the brain, liver, and heart, Pi has been shown to induce mitochondrial reactive oxygen species (ROS) release. Therefore, the purpose of this review article was to gather relevant experimental records of the production of Pi-induced reactive species, mainly ROS, to examine their essential roles in physiological processes, such as the development of bone and cartilage and the development of diseases, such as cardiovascular disease, diabetes, muscle atrophy, and male reproductive system impairment. Interestingly, in the presence of different antioxidants or inhibitors of cytoplasmic and mitochondrial Pi transporters, Pi-induced ROS production can be reversed and may be a possible pharmacological target. Full article
(This article belongs to the Special Issue Phosphate-Related Disorders: From Physiology to Diseases)
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