Nickan Research Institute Journal of Parathyroid Disease 2345-6558 14 1 2026 01 01 Cross-talk of bone remodeling and cardiac dysfunction; reimagining the bone-heart axis in atherosclerosis pathogenesis e13317 e13317 10.34172/jpd.2026.13317 EN Kianoush Saberi https://orcid.org/0000-0002-4292-2252 Amir Heidari https://orcid.org/0000-0001-9802-7487 Mohammad Rostamzadeh https://orcid.org/0009-0004-6817-7467 Abdolmohammad Ranjbar https://orcid.org/0000-0003-2235-2149 Faezeh Nesaei https://orcid.org/0009-0004-4495-0398 Mohammad Parsa Mahjoob https://orcid.org/0000-0003-1269-3134 Iman Zafar Asoodeh https://orcid.org/0009-0003-1347-3827 Reza Faramarzzadeh https://orcid.org/0000-0002-3201-5261 Shahnaz Sharifi https://orcid.org/0000-0001-9194-3538 Journal Article 10.34172/jpd.2026.13317 2025 01 01 2026 02 08 Recent findings detected a dynamic, reciprocal relationship between bone remodeling and cardiac dysfunction, significantly influencing atherosclerosis pathogenesis. The bone-heart axis consists of bidirectional signaling of bone-derived factors and dysregulated mineral metabolism, which directly affect vascular calcification, endothelial function, and myocardial stress. Conversely, cardiac hormones and systemic inflammation modulate osteoclast/osteoblast activity. Critically, shared molecular pathways, like RANKL/RANK/OPG modulate both skeletal turnover and vascular inflammation/calcification. Pathological bone resorption releases calcium and matrix vesicles that nucleate vascular calcification, accelerating atherosclerotic plaque instability. Reimagining this axis emphasizes on osteo-immunological mechanisms with central role in cardiovascular disease progression, suggesting integrated therapeutic targets for atherosclerosis beyond traditional lipid-centric approaches.