SMYD1 alleviates septic myocardial injury by inhibiting endoplasmic reticulum stress.

Sepsis-induced cardiomyopathy (SIC) is a major complication of sepsis. SET and MYND domain containing 1 (SMYD1) has central importance in heart development, and its role in SIC has not been identified. Herein, we found that the expression of SMYD1 was downregulated in myocardial tissues of SIC patients (from GEO database: GSE79962) and lipopolysaccharide (LPS)-induced SIC rats, and LPS-induced H9c2 cardiomyocytes. We used LPS-stimulated H9c2 cells that mimic sepsis in vitro to explore the function of SMYD1 in SIC. MTT assay, LDH and CK-MB release assay, flow cytometry, and ELISA assay showed that SMYD1 overexpression enhanced cell viability, alleviated cell injury, impeded apoptosis, and reduced the level of proinflammatory factors and NF-κB activation under the condition of LPS stimulation. Moreover, SMYD1 exerted protective effect on H9c2 cells stimulated with LPS through relieving endoplasmic reticulum (ER) stress. In conclusion, overexpression of SMYD1 alleviates cardiac injury through relieving ER stress during sepsis.