Yu Hirokawa^1,2, Hirotomo Ten³, Keisuke Onoda^1,2 and Akira Matsuno^1,2,4*

¹Department of Neurosurgery, International University of Health and Welfare, Narita Hospital, Chiba, Japan
²Graduate School of Medicine, International University of Health and Welfare, Chiba, Japan
³Department of Judo Physical Therapy, Faculty of Health Care, Teikyo Heisei University, Tokyo, Japan
⁴Department of Neurosurgery, Teikyo University Chiba Medical Center, Chiba, Japan

*Corresponding Author: Akira Matsuno, Department of Neurosurgery, International University of Health and Welfare, Narita Hospital, Chiba, Japan.

Received: October 25, 2022; Published: November 23, 2022

Abstract

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.

Keywords:Vascular Calcification; Atherosclerosis; Bone Metabolic Marker Protein

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Citation

Citation: Akira Matsuno., et al. “Role of Bone Metabolic Marker Proteins in Calcified Lesions of Carotid Arteriosclerosis". Acta Scientific Neurology 5.12 (2022): 73-79.

Copyright

Copyright: © 2022 Akira Matsuno., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.