Key result
SBF2-AS1 knockdown reduces post-MI cardiomyocyte apoptosis and inflammation by targeting the miR-149-5p/PHLPP2 axis.
Why the study?
LncRNAs regulate cardiomyocyte apoptosis, inflammation, and oxidative stress after AMI through ceRNA mechanisms, but the underlying networks remain incompletely defined.
p-value: p=<0.001
SBF2-AS1 silencing mitigates post-AMI myocardial apoptosis, inflammation, and oxidative stress via the miR-149-5p/PHLPP2 axis, presenting a potential novel therapeutic target for post-infarction remodeling.
SBF2-AS1 inhibition attenuates post-AMI injury in mice; leaves open whether the axis offers a viable human therapeutic target.
Acute myocardial infarction (AMI) triggers cardiomyocyte apoptosis, inflammation, and oxidative stress, contributing to cardiac dysfunction. LncRNAs regulate these processes through competing endogenous RNA (ceRNA) mechanisms, though the underlying networks remain incompletely defined. This study investigated whether SBF2-AS1 contributes to AMI-induced myocardial injury via a ceRNA-dependent pathway and identified the downstream regulatory axis. AMI was induced in C57BL/6 mice by left anterior descending coronary artery ligation. SBF2-AS1 was knocked down via lentiviral injection. Myocardial tissues from the infarct border zone were collected on day 7 for apoptosis analysis and gene expression profiling. In vitro, HL-1 cardiomyocytes were exposed to hypoxia/reoxygenation (H/R). Cell viability, apoptosis, inflammatory cytokines, and oxidative stress markers were assessed. Dual-luciferase reporter assays validated direct molecular interactions. SBF2-AS1 expression was elevated in AMI mouse myocardium. Its knockdown reduced cardiomyocyte apoptosis and suppressed injury markers, pro-inflammatory cytokines, and fibrosis-related genes. In H/R-treated HL-1 cells, SBF2-AS1 silencing improved viability and reduced apoptosis, along with decreased inflammatory cytokine secretion and improved oxidative stress indicators. Luciferase assays confirmed direct binding between miR-149-5p and SBF2-AS1/PHLPP2. Functional rescue experiments showed that miR-149-5p inhibition partially reversed the protective effects of SBF2-AS1 knockdown, while PHLPP2 silencing alleviated the damage caused by miR-149-5p inhibition. In conclusion, SBF2-AS1 promotes cardiomyocyte apoptosis, inflammation, and oxidative stress following AMI by sponging miR-149-5p to upregulate PHLPP2. The SBF2-AS1/miR-149-5p/PHLPP2 axis may represent a novel therapeutic target for AMI.
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Zhang et al. (2026) studied Acute myocardial infarction (n=60). SBF2-AS1 knockdown (sh-SBF2-AS1) vs. Sham surgery or negative control lentivirus (sh-NC) was evaluated on Cardiomyocyte apoptosis, inflammation, and oxidative stress markers (p=<0.001). SBF2-AS1 knockdown significantly reduced cardiomyocyte apoptosis, inflammation, and oxidative stress following acute myocardial infarction by sponging miR-149-5p to upregulate PHLPP2.
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