The role of calprotectin in vascular calcification

Vascular calcification significantly contributes to cardiovascular morbidity and mortality, particularly in high-risk populations like chronic kidney disease (CKD) patients. Calprotectin, a heterodimeric protein with pro-inflammatory and pro-calcific properties, has emerged as a key molecule in vascular pathology. This review highlights the mechanisms linking calprotectin to vascular calcification, its clinical relevance, and its potential as a therapeutic target.

Vascular calcification is an active, cell-mediated process involving vascular smooth muscle cell (VSMC) dysfunction, inflammation, matrix remodeling, and cellular senescence. Calprotectin is strongly associated with cardiovascular disease and vascular calcification, particularly in CKD. Mechanistic studies reveal that calprotectin promotes calcification through the activation of RAGE and TLR4 signaling pathways, driving inflammatory cascades. Preclinical studies demonstrate that pharmacological inhibition of calprotectin attenuates vascular calcification in animal models, supporting its potential as a therapeutic target.

Calprotectin is emerging as a promising biomarker and therapeutic target in vascular calcification, particularly in CKD and aging-related vascular diseases. However, further studies are required to clarify its mechanisms and assess the long-term efficacy and safety of calprotectin-targeted therapies. A deeper understanding of calprotectin's multifaceted role could pave the way for innovative therapeutic strategies targeting both inflammation and mineralization in calcification-related vascular diseases.