Key result
Oxyphospholipids and small lipid mediators promote the transition of vascular smooth muscle and valve interstitial cells to an osteoblast-like phenotype, driving cardiovascular calcification.
Why the study?
Understanding the regulation and molecular processes underpinning cardiovascular mineralization is needed to provide mechanistic insights that could lead to novel therapies.
Understanding the role of oxyphospholipids in cardiovascular calcification provides mechanistic insights that could lead to novel therapies for atherosclerotic plaques and calcific aortic valve disease.
May identify oxyphospholipid targets in vascular calcification; leaves open therapeutic translation to atherosclerosis or valve disease.
Mineralization of cardiovascular structures including blood vessels and heart valves is a common feature. We postulate that ectopic mineralization is a response-to-injury in which signals delivered to cells trigger a chain of events to restore and repair tissues. Maladaptive response to external or internal signals promote the expression of danger-associated molecular patterns, which, in turn, promote, when expressed chronically, a procalcifying gene program. Growing evidence suggest that danger-associated molecular patterns such as oxyphospholipids and small lipid mediators, generated by enzyme activity, are involved in the transition of vascular smooth muscle cells and valve interstitial cells to an osteoblast-like phenotype. Understanding the regulation and the molecular processes underpinning the mineralization of atherosclerotic plaques and cardiac valves are providing valuable mechanistic insights, which could lead to the development of novel therapies. Herein, we provide a focus account on the role oxyphospholipids and their mediators in the development of mineralization in plaques and calcific aortic valve disease.
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Chignon et al. (2020) conducted a review in Cardiovascular calcification. Oxyphospholipids and small lipid mediators was evaluated. Oxyphospholipids and small lipid mediators promote the transition of vascular smooth muscle and valve interstitial cells to an osteoblast-like phenotype, driving cardiovascular calcification.
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