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Vascular calcified plaque

Molecular classification
Other
01

Overview

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].

Other names
Calcified plaqueVascular calcificationArterial calcificationCoronary artery calcification (sometimes abbreviated as CAC)
02

Mechanism of action

Lipid lowering (statins); Inhibition of calcium/phosphorus deposition; Modulation of vascular inflammation; Osteoclast-mediated demineralization (emerging)

03

Biological functions

Other (reflects tissue change, not a direct molecular function)
04

Disease associations

Cardiovascular diseaseAtherosclerosisChronic kidney diseaseDiabetes mellitusHypertension
05

Safety considerations

None specific to "vascular calcified plaque" as a target; therapies aimed at modifying calcification pathways may cause electrolyte imbalance, bone loss, or vascular side effects[6].
06

Interacting drugs

Statins

5 more in the full profile.

07

Biomarkers

Coronary artery calcium (CAC) scoreSerum calcium and phosphateInflammatory markers (e.g. CRP, IL-6)

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