Key result
MiR-184-3p overexpression slows atherosclerosis progression in mice by suppressing inflammation and apoptosis.
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MiR-184-3p overexpression suppresses atherosclerosis progression and inflammation in ApoE-/- mice by inhibiting the STAT3/IL-6/IL-1β/TNFα signaling pathway.
To investigate the effects of miR-184-3p on the progression of atherosclerosis (AS) in apolipoprotein E (ApoE) −/− mice. In this study, bioinformatics analysis was used to identify miRNAs specifically expressed in AS and the associated signaling pathways, followed by in vivo and in in vitro experiments. First, 40 male ApoE-/- mice aged 6–8 weeks old were randomly divided into a Control group, Model group, miR-184-3p OE group, and normal diet + miR-184-3p OE group. Plaque morphological and pathological changes were detected by Sirius red staining. Moreover, the protein expressions of endoplasmic reticulum stress (ERS)-related factors, signal transducer and activator of transcription 3 (STAT3), and related inflammatory cytokines were measured by Western blotting. In addition, RAW264.7 macrophages were cultured and assigned into NC (Negative Control), OE (Overexpress), NC + ox-LDL (Negative Control + Oxidized Low-Density Lipoprotein), and OE + ox-LDL (Overexpress + Oxidized Low-Density Lipoprotein) groups, and the expressions of related proteins were measured by Western blotting. Experimental results showed that miR-184-3p inhibited the expression of STAT3, reducing macrophage infiltration and apoptosis. Compared with the Model group, the protein expression of activating transcription factor 4 (ATF4) had no significant change, the protein expressions of t-STAT3, p-STAT3, interleukin-6 (IL-6), Interleukin-1 beta (IL-1β) and tumor necrosis factor-α (TNF-α), Bcl-2 associated X protein (Bax) and Cleaved Caspase-3 were significantly decreased, and the protein expression of Bcl-2 was significantly increased in the miR-184-3p OE group (P < 0.05). MiR-184-3p can suppress the secretion of inflammatory and apoptotic cytokines, thereby delaying the progression of AS and reducing plaque area. This process may be achieved by miR-184-3p through inhibition of the STAT3/IL-6/IL-1β/TNFα signaling pathway.
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Jia et al. (2026) studied Atherosclerosis (n=40). miR-184-3p overexpression vs. Model group was evaluated on Protein expressions of t-STAT3, p-STAT3, IL-6, IL-1β, TNF-α, Bax, Cleaved Caspase-3, and Bcl-2 (p=< 0.05). MiR-184-3p overexpression significantly decreased inflammatory and apoptotic protein expressions (P < 0.05), delaying atherosclerosis progression in ApoE-/- mice.
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