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The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelial‑mesenchymal transition (EndMT) induced by transforming growth factor beta (TGF‑β), was investigated. Human cardiac microvascular endothelial cells were transfected with LV‑LINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively. The cells were then exposed to TGF‑β in serum‑free medium for 48 h to induce EndMT. Flow cytometric analysis, Cell Counting Kit‑8 assay and immunofluorescence staining were performed to examine the cell apoptosis rate, assess cell viability, and identify CD31 + /α‑SMA + double‑positive cells, respectively. Western blotting and reverse transcription‑ quantitative polymerase chain reaction were used to evaluate protein and mRNA expression, respectively. Injury to endothelial cells and EndMT was induced by TGF‑β in a time‑dependent manner. LINC00961 overexpression promoted injury and EndMT, whereas LINC00961 knockdown had the opposite effects. Knockdown of LINC00961 attenuated EndMT and injury to endothelial cells induced by TGF‑β via the PTEN‑PI3K‑AKT pathway. Inhibition of LINC00961 expression may prevent the occurrence of EndMT‑related cardiovascular diseases, such as myocardial fibrosis and heart failure. Therefore, LINC00961 shows potential as a therapeutic target for cardiovascular diseases.

LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway