Liver fibrosis is a central process in chronic liver disease, yet effective antifibrotic therapies remain limited. The mineralocorticoid receptor (MR) is a key regulator of hepatic homeostasis and fibrogenesis, expressed in hepatocytes, hepatic stellate cells (HSCs), macrophages, and liver sinusoidal endothelial cells (LSECs). MR activation—via aldosterone‑dependent and ligand‑independent mechanisms (hypoxia, oxidative stress)—amplifies TGF‑β signalling, ROS generation, and NF‑κB‑driven inflammation, forming a self‑reinforcing fibrogenic network. Preclinical studies show MR antagonists (MRAs) attenuate fibrosis. Clinical evidence remains limited. Nonsteroidal MRAs, particularly finerenone, offer improved selectivity and safety. Future research should focus on patient stratification, validated endpoints, and rigorous safety evaluation.
