Current studies utilizing cecal ligation and puncture (CLP)-induced SA-AKI have demonstrated that TAK-242 can promote mitochondrial biogenesis (62), modulate mitochondrial quality (63), and ameliorate mitochondrial dysfunction (64), thereby inhibiting the TLR4/NF-κB signaling pathway, enhancing renal tissue mitochondrial function, and preventing CLP-induced SA-AKI in rats, providing substantive data support for the treatment of SA-AKI (65). Here, NFKB1 is linked to acute kidney injury.