| Abstrakt: |
A recent study conducted in Guangdong, China, explored the role of histone deacetylase 4 (HDAC4) in sepsis-induced alveolar epithelial cell injury. The researchers found that HDAC4 expression increased in cells stimulated by lipopolysaccharide (LPS), a component of bacterial cell walls. Silencing HDAC4 inhibited inflammatory damage, reduced oxidative stress, decreased cell apoptosis, improved mitochondrial function, and blocked the c-Jun N-terminal kinase (JNK)/activating protein-1 (AP-1) signaling pathway. These findings suggest that interfering with HDAC4 could potentially ameliorate sepsis-induced alveolar epithelial cell injury through the JNK/AP-1 signaling pathway. Further research is needed to explore this potential therapeutic target. [Extracted from the article] |
