Vulnerable plaques are prone to cause acute vascular events such as AMI and stroke, thus presenting an important mortality risk factor. Microcalcification is recognized as a cause of vulnerable plaque formation. Fetuin-A has been identified as a powerful liver-derived circulating inhibitor of vascular and soft-tissue calcification.

Fetuin-A-containing calciprotein particles (CPPs) facilitate the clearance of calcium phosphate nanocrystals from the extracellular fluid, thus being involved in mineral metabolism and related pathological conditions. Lack of fetuin-A causes critical dysregulation of extra-osseous mineralization inhibitors system.

I aim to develop methods of fetuin-A-based theranostics of soft tissue microcalcification using in-house preclinical models. For these purposes, fetuin-A-RANKL fusion protein will be generated in order to cause local osteoclast activation followed by calcium release at ectopic mineralization sites.

Additionally, RFP-labeled fetuin-A will be synthesized and tested on calcification-prone mice. The novel fetuin-A-based theranostics is foreseen to be implemented into clinical practice for microcalcification imaging and non-invasive treatment, especially in CVD/CKD patients.