Key result
Osteopontin was positively immunostained in both calcified and non-calcified areas of carotid atherosclerotic lesions, whereas osteoprotegerin and RANKL were negatively immunostained in all areas.
Observational (n=18)
Vascular calcification in carotid atherosclerosis is an active process resembling bone formation, regulated by specific bone metabolic marker proteins.
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Hypothesis-generating for osteogenic regulation in carotid plaques; leaves open targeted therapies pending higher-level evidence.
Vascular calcification is an important characteristic of atherosclerosis. According to histological analyses, bone formation tends to occur in heavily calcified carotid lesions devoid of ulceration and hemorrhage. Vascular calcification is not a simple degenerative and necrotic process associated with atherosclerosis but an active process similar to bone formation. Proteins involved in regulating skeletal bone formation are present in human atherosclerotic lesions. These proteins include osteoprotegerin and its ligand, bone sialoprotein, bone morphogenetic protein (BMP)-2 and BMP-4, osteocalcin, osteonectin, matrix Gla protein, and osteopontin. These molecules play important roles as active promotors for calcification or decalcification. These molecules are also important in inflammatory mechanisms in atherosclerosis and calcification.
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Hirokawa et al. (2022) conducted an observational in Carotid artery atherosclerosis (n=18). Bone metabolic marker proteins (OPN, OPG, RANKL) vs. Areas without obvious calcification was evaluated on Immunohistochemical expression of OPN, OPG, and RANKL in calcified and non-calcified areas. Osteopontin was positively immunostained in both calcified and non-calcified areas of carotid atherosclerotic lesions, whereas osteoprotegerin and RANKL were negatively immunostained in all areas.
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