ArticleAtherosclerosis plus2026
Calciprotein particles disrupt autophagy in vascular endothelial cells and smooth muscle cells.
Article in Atherosclerosis plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Calciprotein particles (CPPs) act as buffers against mineral overload, but during prolonged mineral stress they convert from the small, amorphous CPP1 form into large, crystalline CPP2. This shift is associated with endothelial dysfunction and arterial stiffness. In this brief report, we assessed the impact of CPPs on autophagy, a key intracellular homeostatic process for maintaining (cardio)vascular health, in human aortic endothelial cells (HAoECs), human aortic smooth muscle cells (HAoSMCs), and murine eGFP-mRFP-LC3 vascular smooth muscle cells (VSMCs). In HAoECs, both CPP1 and CPP2 (100 μg/mL [Ca
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