Inflammation-associated ectopic mineralization

•Inflammatory milieu in ectopic mineralization containing cells (e.g., immune cells and tissue-resident cells) and pro-inflammatory mediators (e.g., cytokines and chemokines) can induce ectopic mineralization.•Ectopic mineralization is formed in inflammatory conditions through different channels: stimulation of osteogenic signaling pathways, regulation of nucleation and assembly of aberrant calcification.•Anti-inflammatory therapies in reversing and preventing ectopic mineralization are scanty but necessary.•Understanding the cellular and molecular mechanisms that inflammatory insults play in ectopic mineralization contributes to advancing diagnosis and treatments. Ectopic mineralization refers to the deposition of mineralized complexes in the extracellular matrix of soft tissues. Calcific aortic valve disease, vascular calcification, gallstones, kidney stones, and abnormal mineralization in arthritis are common examples of ectopic mineralization. They are debilitating diseases and exhibit excess mortality, disability, and morbidity, which impose on patients with limited social or financial resources. Recent recognition that inflammation plays an important role in ectopic mineralization has attracted the attention of scientists from different research fields. In the present review, we summarize the origin of inflammation in ectopic mineralization and different channels whereby inflammation drives the initiation and progression of ectopic mineralization. The current knowledge of inflammatory milieu in pathological mineralization is reviewed, including how immune cells, pro-inflammatory mediators, and osteogenic signaling pathways induce the osteogenic transition of connective tissue cells, providing nucleating sites and assembly of aberrant minerals. Advances in the understanding of the underlying mechanisms involved in inflammatory-mediated ectopic mineralization enable novel strategies to be developed that may lead to the resolution of these enervating conditions. [Display omitted]