IgA nephropathy is an autoimmune kidney disease characterized by glomerular deposition of galactose-deficient IgA1. Its pathogenesis is primarily attributed to the "multi-hit hypothesis", encompassing mucosal immune abnormalities, formation of immune complexes, complement activation, and renal fibrosis. Recent studies have demonstrated that in the pathogenesis of IgA nephropathy, hyperactivation of the mammalian target of rapamycin (mTOR) signaling pathway could promote mesangial cell proliferation, suppressing autophagy, and exacerbating fibrosis. This article reviewed the progress in the study of the role of mTOR signaling pathway in the pathogenesis of IgA nephropathy, and explored its potential as a therapeutic target of IgA nephropathy.