Phosphate is an essential macromineral often introduced to the body through dietary intake. The mechanisms for maintaining phosphate levels are tightly controlled via hormonal interactions and excretion via the kidneys. However, western diets consist of high levels of inorganic phosphate, which can overwhelm the regulatory mechanisms in place for maintaining homeostasis. Recent studies have found that phosphate burden can lead to activation of inflammatory signaling in various parts of the body. In addition, individuals with impaired kidney function may also experience exacerbated symptoms of phosphate overload due to decreased filtration and elimination. Many disease states can arise as a result of phosphate burden and subsequent inflammatory signaling, including cardiovascular diseases, tumorigenesis, depression, and neuronal disorders. While the pathophysiological causes of these diseases have been elucidated, there remains a need to address the clinical impacts of excessive dietary phosphate intake and to clarify potential drug candidates that may help alleviate these conditions. This brief chapter looks to explain the overall connection between phosphate burden and inflammation in various diseases.
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http://dx.doi.org/10.1007/978-3-030-91623-7_2 | DOI Listing |
Atherosclerosis
February 2025
Department of Clinical Science, Intervention and Technology (CLINTEC), Division of Renal Medicine, Karolinska Institutet, Stockholm, Sweden.
Introduction: Components of both the innate and adaptive immune system impact on arterial walls in atherosclerosis. Fibroblast growth factor-23 (FGF23) is a phosphate regulating hormone linked to cardiovascular disease (CVD) in patients with and without chronic renal disease. However, it remains controversial whether FGF23 is merely a biomarker or contributes to CVD.
View Article and Find Full Text PDFUrol Ann
January 2025
Department of Urology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Introduction: Calculous formation is a well-known complication of lower urinary tract reconstruction using an intestinal segment. Special considerations are required as access to the reconstructed bladder is complicated. To date, a standard strategy is yet to be accepted.
View Article and Find Full Text PDFTher Apher Dial
March 2025
Division of Nephrology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Background: Phosphate binders (PBs) are commonly prescribed to reduce serum phosphate levels. This study examined the association between the PB pill burden and cardiovascular events in hemodialysis patients.
Methods: This retrospective cohort study included 395 patients undergoing hemodialysis between August 2018 and November 2023 at a single facility in Japan.
Parasit Vectors
February 2025
MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu, People's Republic of China.
Background: Trehalose-6-phosphate synthase (HcTPS) and trehalose-6-phosphate phosphatase (HcGOB) are key enzymes for trehalose synthesis in Haemonchus contortus. In addition, previous studies have also demonstrated that HcTPS and HcGOB can regulate the function of host immune cells in vitro, and are important immunosuppressive molecules. Therefore, this study evaluated the potential of HcTPS and HcGOB as vaccine candidates through in vitro and in vivo experiments.
View Article and Find Full Text PDFbioRxiv
January 2025
Division of Hematology, Oncology, and Stem Cell Transplant and Regenerative Medicine, Department of Pediatrics, Stanford University, CA.
Relapse continues to limit survival for patients with B-cell acute lymphoblastic leukemia (B-ALL). Previous studies have independently implicated activation of B-cell developmental signaling pathways and increased glucose consumption with chemo-resistance and relapse risk. Here, we connect these observations, demonstrating that B-ALL cells with active signaling, defined by high expression of phosphorylated ribosomal protein S6 ("pS6+ cells"), are metabolically unique and glucose dependent.
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