Key result
This review summarizes the underlying molecular mechanisms of acute coronary syndrome, highlighting the roles of the NLRP3 inflammasome, noncoding RNAs, and various signaling pathways in its pathogenesis.
Why the study?
Despite landmark developments and rapid refinement in the understanding of ACS, questions remain regarding its pathogenesis, requiring a summary of its underlying causes to enable more effective clinical management.
This review highlights the complex molecular networks, including NLRP3 inflammasomes and noncoding RNAs, that drive the pathogenesis of acute coronary syndrome and offer potential therapeutic targets.
Cardiovascular diseases (CVD) comprise of various heart and blood vessels-related diseases. Acute coronary syndrome (ACS) is one of them. Basic researchers and cardiologists have witnessed landmark developments related to ACS and despite rapid refinement in our understanding; scientists are seeking answers for more questions. Scientists have mapped wide ranging proteins and intricate protein networks which play central role in the pathogenesis in ACS. In this review, we have attempted to summarize underlying causes of ACS. Better understanding of the disease pathology will enable us to get a step closer to an effective clinical management.
No takes yet. Share an insight, caveat, or question.
Balashkevich et al. (2022) conducted a review in Acute coronary syndrome. This review summarizes the underlying molecular mechanisms of acute coronary syndrome, highlighting the roles of the NLRP3 inflammasome, noncoding RNAs, and various signaling pathways in its pathogenesis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: