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High-Density Lipoproteins at the Interface between the NLRP3 Inflammasome and Myocardial Infarction
Helison R P Carmo1, Isabella Bonilha1, Joaquim Barreto1
1Atherosclerosis and Vascular Biology Laboratory (Aterolab), Division of Cardiology, State University of Campinas (UNICAMP), Campinas 13084-971, SP, Brazil.
Insights
High-density lipoproteins (HDL) may mitigate myocardial infarction (MI) injury by modulating NLRP3 inflammasome activation, a key driver of cell death following reperfusion. This review explores HDL
Area of Science:
- Cardiovascular Research
- Immunology
- Cell Death Mechanisms
Background:
- Myocardial infarction (MI) continues to cause high morbidity and mortality, linked to reperfusion injury.
- Reperfusion triggers detrimental cellular events, including oxidative stress, inflammation, and programmed cell death pathways like pyroptosis.
- Pyroptosis is mediated by the NLRP3 inflammasome, a critical inflammatory complex.
Purpose of the Study:
- To review the role of inflammasome activation in myocardial infarction.
- To analyze how high-density lipoproteins (HDL) modulate NLRP3 inflammasome activation post-MI.
Main Methods:
- Comprehensive literature review on inflammasome activation and HDL function in myocardial infarction.
- Analysis of existing research on the interplay between HDL components and NLRP3 inflammasome signaling.
Main Results:
- NLRP3 inflammasome activation is a significant contributor to myocardial injury and cell death following reperfusion.
- High-density lipoproteins (HDL) possess components that can either promote or inhibit NLRP3 inflammasome activation.
Conclusions:
- Targeting NLRP3 inflammasome activation presents a potential therapeutic strategy for reducing MI-related damage.
- HDL's modulatory effects on the NLRP3 inflammasome warrant further investigation for novel MI treatment development.
Abstract:
Despite significant therapeutic advancements, morbidity and mortality following myocardial infarction (MI) remain unacceptably high. This clinical challenge is primarily attributed to two significant factors: delayed reperfusion and the myocardial injury resulting from coronary reperfusion. Following reperfusion, there is a rapid intracellular pH shift, disruption of ionic balance, heightened oxidative stress, increased activity of proteolytic enzymes, initiation of inflammatory responses, and activation of several cell death pathways, encompassing apoptosis, necroptosis, and pyroptosis. The inflammatory cell death or pyroptosis encompasses the activation of the intracellular multiprotein complex known as the NLRP3 inflammasome. High-density lipoproteins (HDL) are endogenous particles whose components can either promote or mitigate the activation of the NLRP3 inflammasome. In this comprehensive review, we explore the role of inflammasome activation in the context of MI and provide a detailed analysis of how HDL can modulate this process.
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