Abstract
Background: Despite the advances of current optimal treatment of atherosclerotic disease, the incidence of events after acute coronary syndrome (ACS) remains high. Colchicine, with its well-established pleiotropic anti-inflam- matory effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) thus reducing systemic inflammation. NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitated by cholesterol crystals that are present in all atherosclerosis stages. cytokines are the crucial inflammatory pathway mediators that promote the formation of plaque and instability in the inflammatory cascade. Objective: This review will elaborate on the function of immune cells in atherosclerosis, explain the mechanisms of NLRP3 inflammasome activation in the context of AAI, and address the possible role of colchicine specifically targeting NLRP3 inflammasome and its concomitant downstream mediators in ACS, and provide an overview of current or ongoing studies produced in this area. Discussion : NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitat- ed by cholesterol crystals that are present in all atherosclerosis stages. Subsequent activation of pro-inflammatory pathway mediators that promote the formation of plaque and instability in the inflammatory cascade. A potential advantage of a medication acting through an inflammatory milieu found in atherosclerotic lesions has recently become the need for novel therapeutic options. Colchicine, with its well-established pleiotropic anti-inflammato- ry effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) thus reducing systemic inflammation. Conclusion: Colchicine is a safe and reliable medication for ACS patients, alongside reveal various benefit in reducing inflammation through inhibition of NLRP3 Inflammasome`
Highlights
Inflammation in acute coronary syndrome (ACS) occurs in multiple pathways
The pathogenesis of atherosclerotic plaque formation, progression, and rupture is mainly associated with inflammation, leading to acute clinical events
Monocytes/macrophages and neutrophils are key effectors of the inflammation occurred during acute coronary syndrome
Summary
Despite the advances of current optimal treatment of atherosclerotic disease, the incidence of events after acute coronary syndrome (ACS) remains high. NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitated by cholesterol crystals that are present in all atherosclerosis stages. Discussion : NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitated by cholesterol crystals that are present in all atherosclerosis stages. Subsequent activation of pro-inflammatory cytokines such as interleukin-1β and interleukin-18 will follow. These cytokines are the crucial inflammatory pathway mediators that promote the formation of plaque and instability in the inflammatory cascade. Colchicine, with its well-established pleiotropic anti-inflammatory effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) reducing systemic inflammation. Conclusion: Colchicine is a safe and reliable medication for ACS patients, alongside reveal various benefit in reducing inflammation through inhibition of NLRP3 Inflammasome
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