Objective: To explore the effect of dapagliflozin on pulmonary vascular remodeling and cardiac function in rats with pulmonary hypertension related to left heart failure (PH-LHF) by regulating the bone morphogenetic protein (BMP)/transforming growth factor-β (TGF-β) signaling pathway. Methods: A PH-LHF rat model was established via transverse aortic constriction (TAC) surgery. Rats were randomized into five groups (n=15 each): sham operation, model, low-dose dapagliflozin (1 mg/kg, ig), high-dose dapagliflozin (3 mg/kg, ig), and pathway activator (3 mg/kg dapagliflozin + 10 mg/kg TGF-β activator SRI-011381, ig). After treatment, right ventricular systolic pressure (RVSP) and left ventricular ejection fraction (LVEF) were measured. Right heart catheterization assessed pulmonary hypertension. Pulmonary arteriole pathology was evaluated via HE staining (wall thickness ratio [WT], vascular area ratio [WA]). Victoria blue and Van Giessen staining detected vascular lesions. ELISA measured serum laminin (LN), hyaluronic acid (HA), TGF-β1, and hydroxyproline (HYP). Western blot analyzed TGF-β/BMP pathway proteins. Results: Compared with the sham group, the model group showed pulmonary arteriole thickening, lumen narrowing, lung injury, and elevated RVSP, mPAP, mRVP, WT, WA, collagen fibers, LN, HA, HYP, TGF-β1, p-Smad1/2/3 (P<0.05); LVEF, elastic fibers, and BMPR2 decreased (P<0.05). Low/high-dose dapagliflozin improved vascular remodeling, cardiac function, and fibrosis markers (P<0.05), with high-dose being superior (P<0.05). The pathway activator reversed dapagliflozin’s beneficial effects (P<0.05). Conclusion: Dapagliflozin improves pulmonary vascular remodeling, cardiac function, and fibrosis in PH-LHF rats, likely via inhibiting the TGF-β/BMP pathway.