Objective To investigate the mechanism by which Moshen Formula treats idiopathic membranous nephropathy （IMN） through the regulation of autophagy via the TRPC6 signaling pathway. Methods Forty male SD rats were randomly divided into a control group （n = 8） and a model group （n = 32）. The model group was induced by cationic bovine serum albumin and then further divided into four subgroups： the model subgroup， the Moshen Formula subgroup， the TRPC6 inhibitor subgroup， and the Moshen Formula + TRPC6 agonist subgroup， with 8 rats in each subgroup. The control group and the model subgroup were administered normal saline by gavage， whereas the other three subgroups were given corresponding drugs for 4 weeks. The general condition of the rats was observed. The levels of serum creatinine， serum albumin， and 24-hour urinary protein were measured. Hematoxylin-eosin （HE） staining was carried out to observe the thickening of the glomerular basement membrane and the infiltration of inflammatory cells. Immunofluorescence was employed to detect the deposition of IgG in the glomeruli. Transmission electron microscopy was utilized to observe the glomerular basement membrane， foot processes， and autophagosomes. Western blot was conducted to detect the expression levels of transient receptor potential cation channel 6 （TRPC6）， microtubule-associated protein 1 light chain 3-Ⅱ （LC3-Ⅱ）， phosphorylated extracellular signal-regulated kinase 1/2 （p-ERK1/2）， phosphorylated mammalian target of rapamycin （p-mTOR）， ubiquitin-binding protein p62， podocin， and phospholipase A2 receptor （PLA2R） in renal tissues. Results Compared with the control group， the rats in the model group exhibited lethargy， a reduction in food intake， loose stools， and dull hair. Additionally， there were significant increases in serum creatinine， a decrease in serum albumin， and an elevation in 24-hour urinary protein （P 0.01）. The expression levels of TRPC6， p-ERK1/2， p-mTOR， p62， and PLA2R were significantly elevated （P 0.01）， whereas the expression levels of LC3-Ⅱ and podocin were decreased （P 0.01）. Renal pathological examination indicated marked thickening of the glomerular basement membrane， interstitial inflammatory infiltration， an increase in IgG deposition， extensive foot-process fusion， disrupted mitochondrial cristae， and impaired autophagy. Compared with the model group， the rats in the Moshen Formula group showed improvements in their general condition， biochemical indicators， and pathological injury. There was a restoration of autophagic flux， a decrease in the expression levels of TRPC6， p-ERK1/2， p-mTOR， and p62 （P 0.01）， and an increase in the expression levels of LC3-II and podocin （P 0.01）. Compared with the Moshen Formula group， the TRPC6 inhibitor group demonstrated more significant decreases in the expression of TRPC6， p-mTOR， and p62 （P 0.05）. However， there were no significant differences in biochemical parameters， podocin， and LC3-Ⅱ expression （P 0.05）. After the combination of the Moshen Formula with a TRPC6 agonist， the pathway-regulating and autophagy-improving effects were attenuated （P 0.05）. Conclusions The Moshen Formula effectively enhances the general condition， biochemical parameters， and alleviates renal pathological damage in rats with IMN. Its mechanism might involve the inhibition of the TRPC6 signaling pathway， the down-regulation of ERK/mTOR， the restoration of autophagic flux， and the up-regulation of podocin. Based on comprehensive phenotypes， the Moshen Formula demonstrated comparable efficacy to a TRPC6 inhibitor. In contrast， the activation of TRPC6 diminished the protective effects of the Moshen Formula， indicating that TRPC6 is a crucial target for the renoprotective action of the Moshen Formula.