AI Article Synopsis
- The NLRP3 inflammasome is a key part of the innate immune system, which gets activated by pattern recognition receptors and leads to the production of inflammatory cytokines like IL-1β and IL-18, resulting in a type of cell death called pyroptosis.
- Recent findings show that excessive activation of the NLRP3 inflammasome contributes to inflammation and the development of atherosclerosis, a condition that affects the arteries.
- The review focuses on the mechanisms of NLRP3 activation and explores potential treatments, including the use of statins and natural medications, to inhibit the inflammasome and treat atherosclerosis.
Article Abstract
The NLRP3 inflammasome is a crucial constituent of the body's innate immune system, and a multiprotein platform which is initiated by pattern recognition receptors (PRRs). Its activation leads to caspase-1 maturation and release of inflammatory cytokines, interleukin-1β (IL-1β) and IL-18, and subsequently causes pyroptosis. Recently, the excess activation of NLRP3 inflammasome has been confirmed to mediate inflammatory responses and to participate in genesis and development of atherosclerosis. Therefore, the progress on the discovery of specific inhibitors against the NLRP3 inflammasome and the upstream and downstream inflammatory factors has become potential targets for clinical treatment. Here we review the recently described mechanisms about the NLRP3 inflammasome activation, and discuss emphatically the pharmacological interventions using statins and natural medication for atherosclerosis associated with NLRP3 inflammasome.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9045366 | PMC |
| http://dx.doi.org/10.3389/fcell.2022.823387 | DOI Listing |
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