Increased C-reactive protein expression exacerbates left ventricular dysfunction and remodeling after myocardial...

Area of Science:

• Cardiovascular Biology
• Inflammation Research
• Translational Medicine

Background:

• Serum C-reactive protein (CRP) elevation post-myocardial infarction (MI) is linked to adverse outcomes.
• CRP exhibits proinflammatory and proapoptotic effects, suggesting a pathogenic role in post-MI cardiac remodeling.

Purpose of the Study:

• To investigate the hypothesis that increased CRP expression exacerbates adverse left ventricular (LV) remodeling after MI.
• To elucidate the specific mechanisms by which CRP influences post-MI cardiac pathology.

Main Methods:

• Utilized transgenic mice with human CRP expression (CRP-Tg) and control littermates.
• Induced MI via left coronary artery ligation.
• Assessed LV remodeling, function, apoptosis, inflammation, and molecular markers post-MI.

Main Results:

• CRP-Tg mice exhibited significantly worse LV dilation and function compared to controls post-MI.
• Increased cardiomyocyte hypertrophy, fibrosis, apoptosis, and macrophage infiltration were observed in CRP-Tg mice.
• Elevated monocyte chemotactic protein (MCP)-1 expression and matrix metalloproteinase (MMP)-9 activity were noted in CRP-Tg mice.

Conclusions:

• Increased CRP expression exacerbates LV dysfunction and promotes adverse LV remodeling following MI in a mouse model.
• The deleterious effects of CRP are associated with increased apoptosis, macrophage infiltration, MCP-1, and MMP-9 activity in the infarct border zone.
• CRP plays a direct pathogenic role in the progression of cardiac damage after myocardial infarction.