About the book
Pyrophosphate (PPi) has long been recognized as a by-product of diverse biosynthetic reactions and was initially identified as a key endogenous inhibitor of biomineralization. PPi is synthesized from extracellular ATP by ecto-nucleotide pyrophosphatase/phosphodiesterase from extracellular ATP hydrolysis. Vascular calcification refers to the deposition of calcium phosphate, mainly in the form of hydroxyapatite crystals, in cardiovascular tissues including arteries and myocardium. It is correlated with an elevated risk of cardiovascular disease and myocardial infarction in diabetic patients and in those with chronic kidney disease. Many enzymes implicated in the metabolism of pyrophosphate have been associated with vascular calcifications. Pyrophosphate may also act as a signaling molecule to regulate gene expression. Thus, it is necessary to outline our current insight regarding pyrophosphate metabolism and how it regulates bone mineralization and inhibits harmful soft tissue calcification. Therapies based on pyrophosphate metabolism have been compelling in animal models, including renal failure, and hold hope as promising therapies to prevent vascular calcification. This work intends to summarize recent progress and future directions for the study of pyrophosphate metabolism and how it regulates bone mineralization and prevents harmful soft tissue calcification, how dysregulation of PPi results in human diseases as well as the development of novel molecules and strategies that can interrogate and manipulate the cellular actions of pyrophosphate.