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Purpose of Review <p>This review aims to provide a comprehensive overview of the interplay between cholesterol crystals (CCs), NLRP3 inflammasome activation, and the progression of atherosclerosis.</p> Recent Findings <p>Emerging evidence highlights the critical role of CCs in enhancing plaque inflammation and instability, increasing the risk of rupture or erosion. Early studies focused on the mechanism of lysosomal damage induced by CCs, leading to the release of cathepsin B into the cytoplasm, which in turn triggers NLRP3 inflammasome activation. More recent studies suggest that the trafficking of cholesterol within macrophages activates NLRP3 via CaMKII/JNK signaling, and NLRP3 deubiquitylation. The activation of the complement system by CCs can also contribute to NLRP3 inflammasome activation via changes in mitochondrial energy metabolism and ROS production worsening atherosclerosis.</p> Summary <p>CCs can aggravate atherosclerosis by triggering a complex interplay of pathways, including lysosomal damage, cholesterol trafficking to ER, and complement system activation, all of which converge on the activation of the NLRP3 inflammasome, driving plaque inflammation and instability.</p>

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Cholesterol Crystals as Triggers of NLRP3 Inflammasome Activation in Atherosclerosis

  • 期刊论文

  • 发表日期：

    2025年8月1日

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  • Mustafa Yalcinkaya,
  • Alan R. Tall

摘要

Purpose of Review

This review aims to provide a comprehensive overview of the interplay between cholesterol crystals (CCs), NLRP3 inflammasome activation, and the progression of atherosclerosis.

Recent Findings

Emerging evidence highlights the critical role of CCs in enhancing plaque inflammation and instability, increasing the risk of rupture or erosion. Early studies focused on the mechanism of lysosomal damage induced by CCs, leading to the release of cathepsin B into the cytoplasm, which in turn triggers NLRP3 inflammasome activation. More recent studies suggest that the trafficking of cholesterol within macrophages activates NLRP3 via CaMKII/JNK signaling, and NLRP3 deubiquitylation. The activation of the complement system by CCs can also contribute to NLRP3 inflammasome activation via changes in mitochondrial energy metabolism and ROS production worsening atherosclerosis.

Summary

CCs can aggravate atherosclerosis by triggering a complex interplay of pathways, including lysosomal damage, cholesterol trafficking to ER, and complement system activation, all of which converge on the activation of the NLRP3 inflammasome, driving plaque inflammation and instability.