Molecular basis of acute coronary syndrome

Abstract

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.

Keywords: Acute coronary syndrome; signaling; therapy.

Figure 1

Plasma low-density lipoproteins (LDL) enter through the arterial wall. LDLs accumulate in mononuclear phagocytes through scavenger receptors. Later, lipid-laden macrophage foam cells die. Death of lipid-rich macrophage foam cells resulted in the accumulation of extracellular cholesteryl ester and cholesterol monohydrate crystals in the lipid-enriched necrotic cores of the plaque. Cholesterol crystals can trigger the activation of the inflammasome that generates biologically active version of the proinflammatory cytokines Interleukin-1 β (IL-1) and IL-18