OBJECTIVES: Hypertension poses a great health threat globally. We probed the mechanisms of long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) mediating ventricular remodeling (VR) in spontaneously hypertensive rats (SHR). METHODS: PVT1 was down-regulated or miR-30a was inhibited in SHR in vivo. Hypertensive injury model was established in vitro. VR, fibrosis and autophagy-related indicators were detected by echocardiography, HE/WGA/Masson staining, ELISA, and immunohistochemistry. Cell viability, fibrosis markers, autophagy-related markers, and lncRNA PVT1 and miR-30a levels were assessed. Interactions between PVT1, Beclin-1 and miR-30a were verified. RESULTS: PVT1 was up-regulated in myocardial tissues of SHR. PVT1 knockdown alleviated VR and myocardial fibrosis (MF) in SHR, as evidenced by decreased systolic blood pressure, left ventricular end-systolic diameter, left ventricular end-systolic diameter, and heart weight index, boosted left ventricular fractional shortening and left ventricular ejection fraction, abated inflammatory infiltration of myocardial tissues, decreased myocardial hypertrophy and interstitial fibrosis, reduced serum angiotensin II (Ang II) and atrial natriuretic peptide, and downregulated collagen I, collagen II, α-smooth muscle actin, and fibronectin protein. PVT1 knockdown down-regulated Beclin 1 and LC3B-II/LC3B-I and up-regulated p62 protein. In vitro, PVT1 knockdown improved fibrosis by inhibiting Ang II-induced cardiomyocyte autophagy. PVT1 acted as a competitive endogenous RNA to competitively bind to miR-30a to target Beclin-1 expression. PVT1 targeted the miR-30a/Beclin-1 axis to mediate autophagy to affect VR and MF in SHR. CONCLUSIONS: LncRNA PVT1 promotes cellular autophagy by targeting the miR-30a/Beclin-1 axis, thereby promoting VR and MF in SHR. Knockdown of lncRNA PVT1 attenuates VR and MF in SHR.