Key result
Overexpression of miR-483-3p significantly reduced the degree of myocardial fibrosis and inhibited cardiomyocyte pyroptosis by targeting FGFR2 via the NLRP3/Caspase-1/GSDMD signaling axis.
Why the study?
The study was conducted to investigate the role of miR-483-3p in reducing myocardial fibrosis and explore its underlying molecular mechanism.
p-value: p=<0.05
Overexpression of miR-483-3p alleviates myocardial fibrosis in rats by targeting FGFR2 and inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway.
Hypothesis-generating for miR-483-3p in myocardial fibrosis; human studies required before clinical consideration.
Purpose In this study, the role of miR-483-3p in reducing myocardial fibrosis (MF) is investigated and the underlying molecular mechanism is further explored. Methods Firstly, six SD rats were randomly divided into sham surgery (Sham) group and model (ISO) group, and high-throughput miRNAs sequencing technology was used to sequence MF model rats. Forty male SD rats were randomly divided into Sham group, ISO group, blank transfection (AAV-NC) group, and overexpression (AAV-miR-483-3p) group, with 10 rats in each group. The MF model was established by tail vein injection of isoprenaline. RT-PCR, Western Blot and immunohistochemical staining were used to detect the expression of miR-483-3p, FGFR2 and cell pyroptosis. Bioinformatics software TargetScan was used to predict targets online and verify with diluciferase reporters; Detection of myocardial fibrosis using HE staining, Masson staining and Western Blot. Results Compared with the ISO group, the degree of MF decreased in the AAV-miR-483-3p group, and the expression of Collagen-1, FGFR2, NLRP3, Caspase-1, GSDMD and IL-1β in cardiomyocytes was significantly reduced. Diluciferase experiments confirmed that FGFR2 is the validated target gene of miR-483-3p. Conclusion miR-483-3p targets FGFR2 to inhibit cell pyroptosis and reduce the degree of MF, possibly via the NLRP3/Caspase-1/GSDMD signaling axis.
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Lv et al. (2023) studied Myocardial fibrosis (n=46). AAV-miR-483-3p (miR-483-3p overexpression) vs. AAV-NC (blank transfection) and ISO (model) group was evaluated on Degree of myocardial fibrosis and expression of pyroptosis-related proteins (p=<0.05). Overexpression of miR-483-3p significantly reduced the degree of myocardial fibrosis and inhibited cardiomyocyte pyroptosis by targeting FGFR2 via the NLRP3/Caspase-1/GSDMD signaling axis.
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