Gut microbiota-derived TMAO drives the kidney-bone-vascular axis in chronic kidney disease complications

the kidneys, and its levels are markedly elevated in CKD patients due to impaired renal function. Studies have demonstrated that TMAO is not only closely associated with an increased risk of vascular calcification but may also exacerbate skeletal disorders in CKD patients by disrupting bone metabolism. This review aims to elucidate the mechanisms underlying TMAO's role in CKD, particularly focusing on its critical involvement in the kidney-bone-vascular axis. Based on existing evidence, we propose potential therapeutic strategies for modulating gut microbiota and TMAO levels, including dietary modifications, probiotic interventions, TMA cleavage enzyme inhibitors, FMO3 inhibitors, and pharmacological regulation, to improve skeletal and cardiovascular health in CKD patients.