Neutrophil Extracellular Traps and NLRP3 Inflammasome: A Disturbing Duo in Atherosclerosis, Inflammation and...

Area of Science:

• Cardiovascular Science
• Immunology
• Pathology

Background:

• Atherosclerosis, a leading cause of global morbidity and mortality, involves arterial plaque formation and blood flow blockage.
• It is driven by pro-inflammatory and pro-coagulatory factors, significantly impacting cardiovascular, rheumatological, and neurological health.
• Neutrophil extracellular traps (NETs) and NLRP3 inflammasome activation are key pathways implicated in its progression.

Purpose of the Study:

• To review the significant roles of NET formation and NLRP3 inflammasome activation in atherosclerosis.
• To elucidate the individual and combined contributions of these processes to inflammation and atherothrombosis.

Main Methods:

• Literature review focusing on the molecular mechanisms of NETs and NLRP3 inflammasome in atherosclerosis.
• Analysis of studies investigating the interplay between these pathways and atherosclerotic plaque development.
• Synthesis of current understanding of their impact on atherothrombosis.

Main Results:

• NET formation contributes to plaque instability and thrombosis.
• NLRP3 inflammasome activation promotes inflammation and cellular dysfunction within atherosclerotic lesions.
• The synergistic action of NETs and NLRP3 inflammasome exacerbates atherosclerotic progression and adverse outcomes.

Conclusions:

• NETs and NLRP3 inflammasome are critical mediators in atherosclerosis, inflammation, and atherothrombosis.
• Targeting these pathways may offer novel therapeutic strategies for managing atherosclerosis.
• Further research is warranted to fully understand their collaborative impact and therapeutic potential.