Berberine attenuates sepsis-associated myocardial injury and mitochondrial dysfunction through the AMPK/PGC-1α/NRF2 signaling pathway.
Mechanistic evidence is provided supporting Ber as a potential modulator of mitochondrial dysfunction during sepsis-associated myocardial injury and mitochondrial regulation as a potential target for further investigation and highlights mitochondrial regulation as a potential target for further investigation.