Journal of cardiothoracic surgery · 2025
Unlocking the therapeutic potential of lncRNA FENDRR in DCM: novel targets and insights via the miR-296-5p/HMGA1 axis.
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Gu Lei, Zhou Zunhai
Аннотация
BACKGROUND: Long non-coding RNA (lncRNA) holds considerable promise in mitigating the onset and progression of diabetic cardiomyopathy (DCM). FENDRR was selected due to its reported involvement in cardiac apoptosis and inflammatory regulation, key pathways in DCM pathogenesis. This study investigated role and underlying mechanisms of FENDRR in DCM.
METHODS: Type 2 diabetes mellitus (T2DM) patients were included and stratified by DCM status. One group was T2DM patients without DCM (n = 49), and the other was T2DM patients with DCM (n = 47).. Clinical data from both groups were compared. qRT-PCR was utilized to quantify serum FENDRR expression, with ROC analysis assessing its diagnostic value. A DCM cell model was established using high glucose-treated H9c2 cells. Flow cytometry and ELISA assays measured apoptosis, myocardial enzyme levels, antioxidant enzyme levels, and inflammatory. Dual-luciferase assays confirmed FENDRR-miR-296-5p and miR-296-5p-HMGA1 interactions.
RESULTS: FENDRR was upregulated in DCM patients and high glucose-treated H9c2s (AUC = 0.888). si-FENDRR mitigated apoptosis in high glucose-stimulated H9c2 cells by inhibiting Bax and promoting Bcl-2 expression. si-FENDRR reduced myocardial enzymes release and inflammatory, and restored antioxidant enzyme levels. miR-296-5p was validated as a target of FENDRR, exhibiting an expression pattern opposite to that of FENDRR. miR-296-5p knockdown negated the positive effects of si-FENDRR on cardiomyocytes. HMGA1, a target gene of miR-296-5p, was upregulated in DCM patients and high glucose environments.
CONCLUSIONS: This preliminary study uncovers the potential diagnostic value of FENDRR in DCM and explores its molecular mechanisms regulating myocardial cell injury via the miR-296-5p/HMGA1 axis.
METHODS: Type 2 diabetes mellitus (T2DM) patients were included and stratified by DCM status. One group was T2DM patients without DCM (n = 49), and the other was T2DM patients with DCM (n = 47).. Clinical data from both groups were compared. qRT-PCR was utilized to quantify serum FENDRR expression, with ROC analysis assessing its diagnostic value. A DCM cell model was established using high glucose-treated H9c2 cells. Flow cytometry and ELISA assays measured apoptosis, myocardial enzyme levels, antioxidant enzyme levels, and inflammatory. Dual-luciferase assays confirmed FENDRR-miR-296-5p and miR-296-5p-HMGA1 interactions.
RESULTS: FENDRR was upregulated in DCM patients and high glucose-treated H9c2s (AUC = 0.888). si-FENDRR mitigated apoptosis in high glucose-stimulated H9c2 cells by inhibiting Bax and promoting Bcl-2 expression. si-FENDRR reduced myocardial enzymes release and inflammatory, and restored antioxidant enzyme levels. miR-296-5p was validated as a target of FENDRR, exhibiting an expression pattern opposite to that of FENDRR. miR-296-5p knockdown negated the positive effects of si-FENDRR on cardiomyocytes. HMGA1, a target gene of miR-296-5p, was upregulated in DCM patients and high glucose environments.
CONCLUSIONS: This preliminary study uncovers the potential diagnostic value of FENDRR in DCM and explores its molecular mechanisms regulating myocardial cell injury via the miR-296-5p/HMGA1 axis.