Fig 2: SIRT2 promotes cartilage damage repair in OA by regulating the NF‐κB/NLRP3 axis. (A) Schematic diagram of the in vivo experimental procedure. (B) Assessment of joint cartilage damage through X‐ray imaging, comparing cartilage structural changes among different treatment groups. (C) Histopathological examination of cartilage tissue using H&E staining to evaluate cartilage damage. (D) Osteoarthritis research society international scoring based on pathological changes in joint tissue for the quantitative evaluation of cartilage damage severity in each group. (E) Immunohistochemical (IHC) staining to detect the expression of cartilage repair markers COL2A1, aggrecan, SOX9, and MMP9 in different treatment groups. (F) Quantitative analysis of the relative expression levels of COL2A1, aggrecan, SOX9, and MMP9, comparing differences among treatment groups. All data are presented as mean ± standard error of the mean. The experiments were performed in triplicate with 10 mice per group. Statistical analysis was conducted using analysis of variance and Tukey's post‐hoc test where *p < 0.05, **p < 0.01, and ***p < 0.001. MMP9, matrix metalloproteinase 9; NF‐κB, nuclear factor kappa B; NLRP3, NOD‐like receptor protein 3; SIRT2, sirtuin 2.

Fig 3: circ_0103896 expression is negatively correlated with IA severity in mice.(A) Representative H&E-stained images showing vessel wall integrity in IA mice subjected to different treatments. (B) Quantification of IA severity based on aneurysmal scores in mice indicated treatments. ∗∗P < 0.01 and ∗∗∗∗P < 0.0001. (C) Grade distribution of aneurysms in IA mice with differential treatments, displayed as pie charts. (D-G) Expression levels of inflammatory mediators, including TNF-α (D), IL1B (E), MMP9 (F), and MMP2 (G), in cerebral arteries of IA mice under the indicated treatments. ∗∗P < 0.01 and ∗∗∗P < 0.001. In vivo data are represented as mean ± SEM, with each mouse representing one biological replicate (n = 6 per group unless otherwise indicated). Aneurysmal scores were analyzed using one-way ANOVA followed by Tukey's post hoc test; The IA grade distributions were analyzed using the chi-square test. ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001. Mice were randomly allocated to groups using a computer-generated sequence stratified by baseline body weight. Histological scoring and grade assignment were performed on coded samples by two independent investigators blinded to treatment groups. Sample sizes (n = 6 per group) were determined a priori based on a power analysis for the aneurysmal score (α = 0.05, power = 0.8, expected mean difference = 1.3, SD = 0.8).

Fig 4: TACSTD2 loss-of-function impedes PTC cell proliferation and migration. A: RT-qPCR and WB verified TACSTD2 mRNA and protein expression in normal human thyroid epithelial cells and PTC cell lines. B: RT-qPCR and WB: The knockdown effect on TACSTD2 following B-CPAP and KTC-1 cell transfection with structured RNA targeting TACSTD2 (LV-sh-TACSTD2#1 and LV-sh-TACSTD2#2) or NC (Lv-sh-NC). C–E: Detection of B-CPAP and KTC-1 cell viability after TACSTD2 silencing assessed via CCK-8, colony formation, and EdU assays. F–H: Evaluating the migration ability of B-CPAP and KTC-1 cells after TACSTD2 silencing by transwell migration/invasion alongside wound healing assays. I: Influence of altered TACSTD2 levels in PTC cells on HLEC tube formation. J–K: WB analysis of metastasis-mediating proteins (MMP-2, MMP-3, MMP-7 and MMP-9) expression in PTC cells following pre-determined transfection.

Fig 5: FTO is regulated by the circ_0103896/miR-432–5p axis in hBVSMCs.(A) Schematic highlighting the predicted binding sites of miR-432–5p within the 3′UTR of FTO. (B) Luciferase essay in hBVSMCs comparing WT and mutant FTO 3′UTRs following miR-432–5p mimic transfection. ∗∗∗P < 0.001. (C-E) FTO expression in hBVSMCs after transfection with circ_0103896 overexpression vectors or miR-432–5p mimics, assessed by RT-qPCR (C) and Western blot (D, E). ∗∗∗P < 0.001. (F-I) Protein expression of α-SMA (F, G), SM22α (F, G), and MMP2 and MMP9 (H, I), in hBVSMCs transfected with circ_0103896 or miR-432–5p mimics. ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001. (J-N) Assessment of hBVSMC proliferation (J), migration (K, L), and apoptosis (M, N) after transfection with FTO plasmids or miR-432–5p mimics, using MTT assay, Transwell migration, and cell apoptosis analysis. ∗∗P < 0.01 and ∗∗∗P < 0.001. Data are represented as mean ± SEM from ≥3 independent biological replicates. qPCR and luciferase assays were performed in technical triplicate. Statistical comparisons were conducted using an unpaired Student's t-test for two-group comparisons or one-way ANOVA with Tukey's post hoc test for multiple groups. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.