Mechanism of NLRP3 Activity and Programmed Cell Death in Cardiovascular Diseases: Pyroptosis
DOI:
https://doi.org/10.5281/zenodo.15105081Keywords:
Pyroptosis, Pyroptosis and cardiovascular diseases, NLRP3, Inflammasome, InflammationAbstract
Cardiovascular diseases are responsible for ~35% of deaths worldwide. Cardiovascular diseases include many conditions that adversely affect the heart and blood vessels, such as hypertension, diabetic cardiomyopathy, obesity, atherosclerosis, myocardial infarction and heart failure. Symptoms of cardiovascular diseases include fatigue, heartbeat disturbances, breathing difficulties and chest pain. Factors that contribute to the development and progression of these diseases include hypercholesterolemia, tobacco use, diabetes and, of course, hypertension. Damage to the heart can induce acute cardiac dysfunction. Damage to the heart can lead to a stereotypical inflammatory response, leading to further dysfunction and increased mortality. The NLRP3 inflammasome has emerged as a central mediator of the inflammatory response to sterile inflammation and tissue damage. NLRP3 components are negligible in the absence of cardiac damage. Studies have demonstrated NLRP3 activity in acute myocardial infarction and activation of NLRP3 leads to an increase in caspase-1 enzyme involved in pyroptosis. In this review, we review studies on the activation of the NLRP3 inflammasome and how this activation affects pyroptosis.
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