Long pentraxin PTX3 exacerbates pressure overload-induced left ventricular dysfunction.

Area of Science:

• Cardiovascular Biology
• Inflammation Research
• Molecular Cardiology

Background:

• Left ventricular hypertrophy is exacerbated by inflammation and cytokines.
• Pentraxin 3 (PTX3) is an inflammatory marker associated with heart failure.
• The role of PTX3 in pressure overload-induced cardiac remodeling is unclear.

Purpose of the Study:

• To investigate the impact of Pentraxin 3 (PTX3) on cardiac hypertrophy and left ventricular dysfunction under pressure overload conditions.

Main Methods:

• Utilized PTX3 knockout (PTX3-KO) and cardiac-specific overexpression (PTX3-TG) mouse models.
• Subjected mice to transverse aortic constriction (TAC) or sham operation.
• Assessed cardiac hypertrophy, left ventricular function, fibrosis, and inflammatory markers.

Main Results:

• Cardiac PTX3 expression increased post-TAC in wild-type mice.
• PTX3 modulated extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor kappa-B (NF-κB) signaling pathways.
• PTX3-KO mice showed attenuated cardiac remodeling and dysfunction, while PTX3-TG mice exhibited exacerbated responses.

Conclusions:

• Pentraxin 3 (PTX3) directly influences hypertrophic responses and ventricular dysfunction.
• PTX3 acts as a key mediator in the cardiac response to increased afterload.