A newly published study reports that a long non-coding RNA called SBF2-AS1 amplifies the damage heart tissue suffers after an acute myocardial infarction, the event commonly known as a heart attack. Researchers found that SBF2-AS1 expression was elevated in the heart muscle of mice after induced infarction, and that silencing this RNA molecule reduced cardiomyocyte apoptosis, inflammation, and oxidative stress, the key processes that drive cardiac dysfunction after such an event.
The investigation, led by Hui Zhang, Yuyan Hou, and Zhifang Wang, was published in Cell Biology and Toxicology as an open-access article. The work focused on competing endogenous RNA mechanisms, a regulatory framework in which long non-coding RNAs act as molecular sponges that bind microRNAs, thereby preventing those microRNAs from interacting with their downstream gene targets.
To test the role of SBF2-AS1 in vivo, the team induced acute myocardial infarction in C57BL/6 mice through ligation of the left anterior descending coronary artery. They then knocked down SBF2-AS1 using lentiviral injection and collected myocardial tissue from the infarct border zone on day seven for apoptosis analysis and gene expression profiling. The results showed that reducing SBF2-AS1 levels suppressed injury markers, pro-inflammatory cytokines, and fibrosis-related genes in the damaged heart tissue.
Complementary experiments were performed in vitro using HL-1 cardiomyocytes exposed to hypoxia/reoxygenation conditions, a laboratory model that mimics the oxygen deprivation and restoration heart cells experience during and after an infarction. In these cells, SBF2-AS1 silencing improved cell viability and reduced apoptosis, while also decreasing inflammatory cytokine secretion and improving oxidative stress indicators.
The molecular pathway underlying these effects was mapped using dual-luciferase reporter assays, which confirmed direct binding between miR-149-5p and both SBF2-AS1 and PHLPP2.
Functional rescue experiments strengthened the evidence for this regulatory axis. When the researchers inhibited miR-149-5p, the protective effects of SBF2-AS1 knockdown were partially reversed. Conversely, silencing PHLPP2 alleviated the damage caused by miR-149-5p inhibition, confirming the causal chain linking the three molecules in a single pathway.
The study concludes that the SBF2-AS1/miR-149-5p/PHLPP2 axis promotes cardiomyocyte apoptosis, inflammation, and oxidative stress following acute myocardial infarction. The authors suggest that this competing endogenous RNA network may represent a novel therapeutic target for AMI, offering a potential direction for future interventions aimed at limiting myocardial injury after ischemic events.
Subject of Research: The role of the lncRNA SBF2-AS1/miR-149-5p/PHLPP2 axis in myocardial injury following acute myocardial infarction.
Article Title: LncRNA SBF2-AS1 exacerbates myocardial injury following acute myocardial infarction by miR-149-5p/PHLPP2
Article References: Zhang, H., Hou, Y., & Wang, Z. (2026). LncRNA SBF2-AS1 exacerbates myocardial injury following acute myocardial infarction by miR-149-5p/PHLPP2. Cell Biology and Toxicology. https://doi.org/10.1007/s10565-026-10282-0
Image Credits: AI Generated
DOI: 10.1007/s10565-026-10282-0
Keywords: SBF2-AS1, acute myocardial infarction, miR-149-5p, PHLPP2, cardiomyocyte apoptosis, ceRNA mechanism, oxidative stress, inflammation, hypoxia/reoxygenation, long non-coding RNA, heart injury, therapeutic target
News Source: Drew Townsend. (October 29, 2026). LncRNA SBF2-AS1 Worsens Heart Injury After Attack via miR-149-5p/PHLPP2 Axis. Scienmag.
