Description
Title: Cardiovascular calcification is coordinated by biomolecules.
Abstract: Vascular calcification, once thought to be a degenerative, terminal, and inevitable condition, is now understood to be a complex process regulated at the molecular and cellular levels similarly to skeletal bone. Decades of research since the original identification of bone morphogenetic protein in calcified human atherosclerotic lesions have now led to the understanding that the regulatory mechanisms and biomolecules that regulate cardiovascular calcification also regulate skeletal mineralization. In this review, we concentrate on the crucial biomolecules that are responsible for ectopic calcification in the circulation and how metabolic, hormonal, and inflammatory stimuli control them. The net risk of plaque rupture and subsequent cardiac events depends on the local material strength even though calcium deposits in the vessel wall increase rupture stress at the edges facing applied tensile stress while simultaneously reducing rupture stress at the orthogonal edges. Therapeutic agents intended to inhibit vascular calcification may adversely affect skeletal mineralization and vice versa, which is a clinically significant result of the shared mechanisms between the vascular and bone tissues. Therefore, when creating therapeutic strategies, both systems must be taken into account.
Keywords: cardiovascular; calcification; inflammation; lipids; skeletal
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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