COVIDâ19 is mainly characterized by respiratory disorders and progresses to multiple organ involvement in severe cases. With expansion of COVIDâ19 and SARSâCoVâ2 research, correlative liver injury has been revealed. It is speculated that COVIDâ19 patients exhibited abnormal liver function, as previously observed in the SARS and MERS pandemics. Furthermore, patients with underlying diseases such as chronic liver disease are more susceptible to SARSâCoVâ2 and indicate a poor prognosis accompanied by respiratory symptoms, systemic inflammation, or metabolic diseases. Therefore, COVIDâ19 has the potential to impair liver function, while individuals with preexisting liver disease suffer from much worse infected conditions. COVIDâ19 related liver injury may be owing to direct cytopathic effect, immune dysfunction, gutâliver axis interaction, and inappropriate medication use. However, discussions on these issues are infancy. Expanding research have revealed that angiotensin converting enzyme 2Â (ACE2) expression mediated the combination of virus and target cells, iron metabolism participated in the virus life cycle and the fate of target cells, and amino acid metabolism regulated immune response in the host cells, which are all closely related to liver health. Further exploration holds great significance in elucidating the pathogenesis, facilitating drug development, and advancing clinical treatment of COVIDâ19ârelated liver injury. This article provides a review of the clinical and laboratory hepatic characteristics in COVIDâ19 patients, describes the etiology and impact of liver injury, and discusses potential pathophysiological mechanisms.