The gut microbiota plays a crucial role in liver regeneration. Preliminary studies in mice have shown that liver cell proliferation post-partial hepatectomy is associated with significant changes in gut microbiota composition, with a relative increase of Bacteroidetes and a decrease of Firmicutes. These changes are thought to facilitate liver regeneration by modifying gut mucosal epithelial barrier permeability and affecting metabolite release. After partial hepatectomy in rodents, most liver mass is restored within 7–8 days, with complete restoration achieved within 3 weeks. Reduced liver regeneration rates have been observed in germ-free mice compared to controls, with recolonization of germ-free mice with normal gut microbiota restoring liver regeneration rates. Similarly, antibiotic-treated mice show reduced liver regeneration, which can be mitigated by probiotics or fecal microbiota transplantation. Human patients who received probiotics and prebiotics post-hepatectomy had higher liver function capacity, lower postoperative infection rates, hospitalization stays, and antibiotic usage compared to controls. Also, gut microbiota-derived molecules, such as lipopolysaccharides, bile acids, short-chain fatty acids, and tryptophan derivatives, play a critical role in liver regeneration. Lipopolysaccharides, produced by enteric gram-negative bacteria, bind to Toll-like receptor 4 in liver cells, activating NF-𝜅B and promoting the production of tumor necrosis factor 𝛼 and interleukin-6, which stimulate hepatic stellate cells to generate hepatocyte growth factor, leading to hepatocyte regeneration. This inflammation-driven regeneration ceases once the liver sufficiently regenerates. Bile acids play an ambivalent role in liver regeneration. Excessive intrahepatic bile acid levels can injure hepatocytes, while reduced levels hamper regeneration. Gut microbiota modifies bile acid solubility, facilitating their recirculation to the liver. During liver regeneration, reduced levels of Firmicutes, particularly Clostridia, which are involved in bile acid deconjugation, may impact this process. Short-chain fatty acids and tryptophan derivatives were shown to enhance liver regeneration by strengthening the gut epithelial barrier and inducing other regenerative molecules such as insulin, triiodothyronine, and glucagon-like-peptide-1. In conclusion, gut microbiota and its derived molecules significantly influence liver regeneration, with potential therapeutic implications for enhancing post-injury liver recovery through microbiota modulation.