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Vascular calcified plaque refers to the accumulation of calcium within atherosclerotic plaques in the vessel walls, typically in the arteries. This calcification is a hallmark of advanced atherosclerosis and is a pathological process whereby mineral (mainly hydroxyapatite crystals) deposits in the intimal or medial layers of arteries[3][7]. Calcified plaques contribute to arterial stiffening, reduce vascular compliance, and are significant predictors of cardiovascular risk, including heart attack and stroke[1][5][7]. Vascular calcification is an active, regulated process involving vascular smooth muscle cell (VSMC) phenotypic switches, extracellular vesicles (especially matrix vesicles), inflammation, and metabolic disturbances[2][6]. While measuring vascular calcified plaque (e.g., through coronary artery calcium scoring) is highly valuable for risk prediction, it is not itself a molecular target (such as a receptor or enzyme), but rather a pathological outcome of multiple molecular pathways and cellular processes[4][3][2]. Therapeutic targeting focuses on the underlying drivers (like inflammation, mineral metabolism, VSMC activity) or preventing further calcification and plaque progression. Important note: "Vascular calcified plaque" is not a canonical therapeutic target or single molecular entity (like a receptor or enzyme)[3][2]; instead, it is a clinical/pathological feature resulting from multiple underlying processes. For drug development, attention is on molecular mediators involved in its formation (e.g., regulators of mineral metabolism, inflammation, or VSMC transdifferentiation)[4][6]. Summary of mapping conventions: - The term represents a clinical/pathological entity, not a distinct molecular target. - For structured data extraction or pharmacological databases, list as not a target and flag as "incorrect" for direct targeting. - Underlying molecular mediators (e.g., matrix vesicles, RUNX2, Bone morphogenetic proteins, etc.) are current and emerging targets for therapies against vascular calcification, but not the plaque itself[2][4][6].
Lipid lowering (statins); Inhibition of calcium/phosphorus deposition; Modulation of vascular inflammation; Osteoclast-mediated demineralization (emerging)
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