Collectively, these results indicate that HSPA12A interacts with PGC-1α and increases its nuclear translocation, thereby inducing AOAH expression for cytosolic LPS inactivation, which ultimately leading to inhibition of the Caspase-11-mediated pyroptosis of hepatocytes that manifested reduced liver injury and improved systemic conditions during endotoxemia (Fig. 8f). Here, PPARGC1A is linked to serum lipopolysaccharide activity.