Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention

Article Title: Effects of PCSK9 inhibitors on vascular function, lipid profile, and cardiovascular outcomes in patients with peripheral artery disease: A systematic review and meta-analysis

doi: 10.1016/j.ijcrp.2026.200590

Figure Lengend Snippet: Summary of included studies.

Article Snippet: Clavijoa, 2023 , RCT, Double-blind , USA , 6 months , Evolocumab 420 mg SC q4w , placebo , 35 , 35 , 70 , Patients aged 40–85 years with a diagnosis of atherosclerotic cardiovascular disease and PAD (Rutherford class I-VI), confirmed by an ankle-brachial index (ABI) ≤0.9 at rest or ≤0.8 after exercise, angiography, duplex ultrasound, or a history of lower extremity surgical or endovascular revascularization. Patients had to be at least one month from their most recent intervention, stable on maximal tolerated lipid-lowering therapy for at least four weeks, and have a fasting LDL cholesterol ≥55 mg/dL or non-HDL cholesterol ≥80 mg/dL. , MWT at 6 months , After six months, Evolocumab significantly improved MWT, FMD, Carotid IMT, and plasma MRP-14 levels. In contrast, changes in pain-free walking time, ABI, TBI, transcutaneous oxygen pressure, oxLDL, and sCD36 were not statistically significant..

Techniques: Control, Biomarker Discovery, Clinical Proteomics, Activation Assay

Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention

Article Title: Effects of PCSK9 inhibitors on vascular function, lipid profile, and cardiovascular outcomes in patients with peripheral artery disease: A systematic review and meta-analysis

doi: 10.1016/j.ijcrp.2026.200590

Figure Lengend Snippet: Summary of included studies.

Article Snippet: Clavijoa, 2023 , RCT, Double-blind , USA , 6 months , Evolocumab 420 mg SC q4w , placebo , 35 , 35 , 70 , Patients aged 40–85 years with a diagnosis of atherosclerotic cardiovascular disease and PAD (Rutherford class I-VI), confirmed by an ankle-brachial index (ABI) ≤0.9 at rest or ≤0.8 after exercise, angiography, duplex ultrasound, or a history of lower extremity surgical or endovascular revascularization. Patients had to be at least one month from their most recent intervention, stable on maximal tolerated lipid-lowering therapy for at least four weeks, and have a fasting LDL cholesterol ≥55 mg/dL or non-HDL cholesterol ≥80 mg/dL. , MWT at 6 months , After six months, Evolocumab significantly improved MWT, FMD, Carotid IMT, and plasma MRP-14 levels. In contrast, changes in pain-free walking time, ABI, TBI, transcutaneous oxygen pressure, oxLDL, and sCD36 were not statistically significant..

Techniques: Control, Biomarker Discovery, Clinical Proteomics, Activation Assay

Journal: iScience

Article Title: Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

doi: 10.1016/j.isci.2026.115151

Figure Lengend Snippet: Nicotine reprograms the miRNA cargo of adipose-derived EVs, with miR-210-3p as a key mediator of macrophage dysfunction (A) Experimental workflow for miRNA sequencing of adipose-derived EVs: EVs were isolated from visceral adipose tissue (VAT) of mice in high-fat diet (HFD) and HFD + nicotine (HFD + Ni) groups. (B) Volcano plot of differentially expressed miRNAs (fold change ≥1.5, p ≤ 0.05) in adipose-derived EVs from HFD +Ni versus HFD mice. (C) Heatmap of the top 20 differentially expressed miRNAs between HFD EVs ( n = 4) and HFD+Ni EVs ( n = 3) isolated from VAT of ApoE −/− mice. (D) RT-qPCR validation of representative differentially expressed miRNAs (e.g., miR-210-3p, miR-192-3p) in adipose-derived EVs from nicotine-treated vs. control ApoE −/− mice ( n = 3). miR-210-3p is highlighted in red. (E) Gene ontology (GO) biological-process enrichment analysis of targets of differentially expressed miRNAs, highlighting processes related to atherogenesis, including macrophage activation, inflammatory cytokine secretion, and foam-cell formation. (F) Expression of miR-210-3p in EVs and cells from nicotine-stimulated 3T3-L1 adipocytes and VAT-derived EVs from HFD-fed mice treated with nicotine (3T3-L1, n = 8; VAT, n = 6). (G) Expression of miR-210-3p in nicotine-stimulated 3T3-L1 adipocytes and VAT from HFD-fed mice treated with nicotine (3T3-L1, n = 8; VAT, n = 6). (H) qRT-PCR analysis of miR-210-3p expression in serum-derived EVs from HFD and HFD+Ni mice ( n = 6). (I) Transfection efficiency of miR-210-3p mimic in RAW264.7 macrophages ( n = 3). (J and K) qRT-PCR analysis of mRNA expression of inflammatory mediators in macrophages transfected with the miR-210-3p mimic (J: IL-6, IL-1β, iNOS, TNF-α, NF-κB, NLRP3, n = 3) or miR-210-3p inhibitor (K: IL-1β, n = 6; IL-6, n = 3). (L and M) Representative fluorescence images and quantification of intracellular ROS levels after miR-210-3p mimic transfection (scale bars, 50 μm; n = 6). (N and O) Representative oil red O staining and quantification of lipid accumulation after miR-210-3p mimic transfection (scale bars, 100 μm; n = 3). (P and Q) BODIPY-cholesterol staining and quantification of lipid accumulation in macrophages transfected with the miR-210-3p mimic (scale bars, 50 μm; n = 6). Values are shown as mean ± SEM. Two-group comparisons were performed using unpaired, two-tailed Student’s t tests, and multi-group comparisons were analyzed by one-way ANOVA followed by Tukey’s multiple-comparisons post-hoc test. Sample sizes (n) indicate biological replicates per group. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Sterol uptake was assessed using BODIPY–cholesterol (MedChemExpress), a fluorescent cholesterol analog.

Techniques: Derivative Assay, Sequencing, Isolation, Quantitative RT-PCR, Biomarker Discovery, Control, Activation Assay, Expressing, Transfection, Fluorescence, Staining, Two Tailed Test

Journal: iScience

Article Title: Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

doi: 10.1016/j.isci.2026.115151

Figure Lengend Snippet: miR-210-3p promotes macrophage inflammatory activation and foam cell formation through KLF7 suppression, which is reversed by KLF7 overexpression (A) Venn diagram showing 10 common downstream target genes of miR-210-3p identified from three databases (TarBase, mirDIP, and TargetScan); KLF7 was selected as a key target for further investigation. Potential binding sites of miR-210-3p on the KLF7 mRNA 3′ untranslated region (3′UTR) (3′UTR) are also shown. (B) Dual-luciferase reporter assay in HEK293T cells co-transfected with miR-210-3p mimics (or NC mimics) and luciferase vectors containing wild-type (Klf7-WT) or Mutant (Klf7-MT) 3′UTR ( n = 9). (C–E) Validation of KLF7 suppression in macrophages. Western blot images (C), quantification of KLF7/GAPDH protein ratio (D, n = 6), and qRT-PCR analysis of Klf7 mRNA (E, n = 3) after transfection with miR-210-3p mimics or inhibitors. (F and G) Representative immunofluorescence images (F) and quantification (G) of KLF7 expression after transfection with miR-210-3p mimics or inhibitors (KLF7, red; nuclei, blue [DAPI]; n = 6; scale bars, 20 μm). (H and I) RT-qPCR (H, n = 6) and western blot (I, n = 3) analyses confirming transduction efficiency and KLF7 overexpression in macrophages following lentiviral transduction with Lv-KLF7 or empty lentivirus (control). (J and K) qRT-PCR analysis of IL-1β and IL-6 mRNA expression in macrophages post-transfection with miR-210-3p mimics and/or transduction with Lv-KLF7 ( n = 6). (L and M) Representative immunofluorescence images (L) and quantification (M) of KLF7 expression in RAW264.7 macrophages transfected with miR-210-3p mimics and transduced with Lv-KLF7 (KLF7, green; nuclei, blue [DAPI]; n = 4; scale bars, 50 μm). (N and O) Representative DCFH-DA fluorescence images (N) and quantification (O) of intracellular ROS levels (green). Red fluorescence (mCherry) indicates macrophages successfully transduced with the lentiviral vectors. Note that KLF7 overexpression attenuates miR-210-3p-induced oxidative stress. (scale bars, 50 μm; n = 6). (P and Q) Representative BODIPY-cholesterol fluorescence images (P) and quantification of intracellular fluorescence intensity (Q) in macrophages transfected with miR-210-3p mimics and transduced with Lv-KLF7 ( n = 3; scale bars, 50 μm). (R and S) Representative oil red O staining (R) and semi-quantitative analysis of oil red O-positive lipid area (S) in macrophages transfected with miR-210-3p mimics and transduced with Lv-KLF7 ( n = 5; scale bars, 100 μm). Values are shown as mean ± SEM. Two-group comparisons were performed using unpaired, two-tailed Student’s t tests, and multi-group comparisons were analyzed by one-way ANOVA followed by Tukey’s multiple-comparisons post-hoc test. Sample sizes (n) indicate biological replicates per group. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Sterol uptake was assessed using BODIPY–cholesterol (MedChemExpress), a fluorescent cholesterol analog.

Techniques: Activation Assay, Over Expression, Binding Assay, Luciferase, Reporter Assay, Transfection, Mutagenesis, Biomarker Discovery, Western Blot, Quantitative RT-PCR, Immunofluorescence, Expressing, Transduction, Control, Fluorescence, Staining, Two Tailed Test

Journal: Materials Today Bio

Article Title: Ultrasound-triggered dissolving microneedle platform for cGAS-STING-mediated precision immunotherapy of melanoma

doi: 10.1016/j.mtbio.2026.102990

Figure Lengend Snippet: Preparation and characterization of ROS-responsive Mn@CTL-LPs. (A) Chemical synthesis of ROS-responsive prodrug Chol-tk-Lin. (B) 1 H NMR characterization of cholesterol, Lin and prodrug Chol-tk-Lin. (C) TEM images of Mn@LPs, CRL-LPs and Mn@CTL-LPs after negative staining with phosphotungstic acid. (D) The particle size and distribution of Mn@CTL-LPs. (E) Mn 2p XPS spectra of Mn@CTL-LPs in PBS and 10 mM GSH. (F) Time-dependent generation of 1 O 2 by Mn@CTL-LPs under US irradiation (1.5 W cm −2 , 5 min), detected using the DPBF probe. (G) Cumulative release profiles of MnTCPP from Mn@CTL-LPs and Mn@LPs in PBS or 1 mM H 2 O 2 . (H) Cumulative release profiles of Lin from Mn@CTL-LPs and CTL-LPs in PBS or 1 mM H 2 O 2 . Bars indicate standard deviation (n = 3).

Article Snippet: Mn (III) Meso-Tetra (4-carboxyphenyl) porphine chloride (MnTCPP), 1,2-Dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and cholesterol were purchased from MedChem Express (Monmouth Junction, NJ, USA).

Techniques: Negative Staining, Irradiation, Standard Deviation