Silica nanoparticles induce JNK-mediated inflammation and myocardial contractile dysfunction

Area of Science:

• Environmental toxicology
• Nanomaterial safety
• Cardiovascular research

Background:

• Growing environmental exposure to silica nanoparticles (SiNPs) necessitates understanding their potential health risks.
• Limited studies exist on the cardiotoxicity of SiNPs, posing challenges for safety assessments.

Purpose of the Study:

• To investigate the adverse effects of subacute SiNP exposure on rat cardiac function.
• To elucidate the underlying molecular mechanisms of SiNP-induced cardiotoxicity.

Main Methods:

• Echocardiography, ultrastructural, and histopathological analyses were performed on rat heart tissues.
• Biochemical assays measured myocardial enzymes, inflammatory factors, and oxidative damage markers.
• Molecular techniques, including lentivirus transfection for JNK knockdown, assessed protein and mRNA expression of key signaling pathways (JNK/TF/PAR1).

Main Results:

• SiNPs induced cardiac contractile dysfunction, characterized by myocardial structural damage, edema, and myocyte apoptosis.
• Increased serum and heart levels of myocardial enzymes, inflammatory factors, and oxidative stress were observed.
• SiNPs upregulated the JNK/TF/PAR1 signaling pathway, which was implicated in F-actin disruption and cardiac dysfunction.

Conclusions:

• SiNPs cause significant cardiotoxicity, leading to impaired heart function and structural damage.
• The JNK/TF/PAR1 signaling pathway plays a critical role in mediating SiNP-induced myocardial contractile dysfunction.
• These findings highlight the importance of evaluating nanoparticle safety, particularly for cardiovascular effects.