SMYD1 alleviates septic myocardial injury by inhibiting endoplasmic reticulum stress

Area of Science:

• Cardiology
• Molecular Biology
• Pathology

Background:

• Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis.
• The role of SET and MYND domain containing 1 (SMYD1) in SIC remains unclear.
• SMYD1 is crucial for cardiac development.

Purpose of the Study:

• To investigate the role and mechanism of SMYD1 in sepsis-induced cardiomyopathy.
• To explore SMYD1's function in a cellular model of sepsis.

Main Methods:

• Analysis of SMYD1 expression in patient and animal models of SIC, and in vitro cell models.
• Utilized lipopolysaccharide (LPS) to induce sepsis in H9c2 cardiomyocytes.
• Assessed cell viability, injury markers (LDH, CK-MB), apoptosis, inflammatory factors, NF-κB activation, and endoplasmic reticulum (ER) stress.

Main Results:

• SMYD1 expression was downregulated in myocardial tissues of SIC patients, SIC rats, and LPS-treated H9c2 cells.
• SMYD1 overexpression improved cell viability, reduced cell injury and apoptosis, and decreased inflammatory factors and NF-κB activation in LPS-stimulated H9c2 cells.
• SMYD1 alleviated ER stress in response to LPS stimulation.

Conclusions:

• SMYD1 plays a protective role in sepsis-induced cardiomyopathy.
• Overexpression of SMYD1 alleviates cardiac injury during sepsis by mitigating ER stress and inflammation.