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Representative histological images of carotid plaques, stained with Hematoxylin and eosin. (A) A stable carotid plaque. No obvious erosion, ulcer, hemorrhage or blood clot, granulocytic or cap macrophage infiltration or plaque rupture was observed. Magnification: left, ×40; right, x200. (B) An unstable carotid plaque. Obvious neovascularization, some with blood clot, clustered lymphocyte infiltration, intraplaque hemorrhage, or cholesterol clefts were observed. Magnification: left, ×40; right, x200
Source publication
Background:
We aimed to determine whether NLRP3 inflammasomes in peripheral blood mononuclear cells (PBMC) were associated with carotid plaque instability in carotid atherosclerosis patients.
Methods:
Consecutive 38 carotid atherosclerosis with vulnerable plaques, 22 carotid atherosclerosis with stable plaques, and 40 healthy subjects with no ca...
Context in source publication
Context 1
... HE staining of stable and unstable carotid atherosclerotic plaques obtained from CEA surgery are shown in Fig. 2. Plaques with vulnerable phenotypes showed larger core filled with more cholesterol clefts, thinner fibrous cap with increased formation of intraplaque hemorrhage, compared to those in stable plaques. Immunohistochemical staining showed that unstable plaques had greater macrophage infiltration and increased number of endothelial or ...
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Citations
... As far as plaque vulnerability is concerned, NLRP3 inflammasome expression was shown to be higher in patients with an ACS, followed by patients with stable angina, compared to those without coronary artery disease [34][35][36], showing a link between plaque vulnerability and clinical outcomes. These findings are in agreement with a recent study that demonstrated a significant correlation between vulnerable carotid atherosclerotic plaques and mRNA or protein expression of NLRP3 inflammasome components when compared to the stable plaque group [37]. Furthermore, the existence of cholesterol crystals in culprit lesions of patients with an acute coronary syndrome (ACS) was correlated with greater mRNA levels of NLRP3 in peripheral blood mononuclear cells, significantly higher concentrations of circulating IL-1β and IL-18, as well as a greater prevalence of thin-cap fibroatheromas, thrombus, plaque rupture, and spotty calcifications, among others, in optical coherence tomography [38]. ...
Atherosclerosis, a chronic inflammatory disease characterized by arterial plaque accumulation, remains a significant global health challenge. In recent years, inflammasomes, the intracellular multiprotein complexes crucial for initiating innate immune responses, have emerged as key players in atherosclerosis pathophysiology. This review article aims to provide a comprehensive overview of the current understanding of inflammasome activation and its impact on atherosclerosis development and progression. We explore the intricate interplay between traditional cardiovascular risk factors and inflammasome activation, leading to the perpetuation of inflammatory cascades that drive plaque formation and instability. The review focuses on the molecular mechanisms underlying inflammasome activation, including the role of pattern recognition receptors and cytokines in this process. Moreover, we discuss the contribution of inflammasomes to endothelial dysfunction, foam cell formation, and vascular inflammation. Additionally, recent advances in therapeutic strategies targeting inflammasomes are examined, including pharmacological agents and potential immunomodulatory approaches. By collating and analyzing the current evidence, this review provides valuable insights into the potential of inflammasome-targeted therapies for atherosclerosis management and treatment. Understanding the pivotal role of inflammasomes in atherosclerosis pathophysiology offers promising prospects for developing effective and personalized therapeutic interventions that can mitigate the burden of this prevalent cardiovascular disorder and improve patient outcomes.
