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: Inhibition of miR-210-3p in atherosclerotic plaques alleviates nicotine-induced atherosclerosis (A) Left: Representative en face images of aortic arch plaques from negative control (NC) and AAV9-anti-miR-210-3p-treated (miR-210-3p inhibition) mice. Right: schematic illustration of the experimental design. ApoE −/− mice were injected with either AAV9-NC inhibitors or AAV9–miR-210-3p inhibitors, followed by HFD+Ni treatment for 12 weeks before analysis (scale bars, 1mm). (B and C) H&E-stained sections of aortic sinuses from nicotine-treated ApoE −/− mice and corresponding quantification of lesion area ( n = 8; scale bars, 200 μm). (D and E) Oil red O-stained sections of aortic sinuses and quantification of oil red O-positive area ( n = 4; scale bars, 200 μm). (F–M) Immunohistochemical staining and corresponding quantification of SOD2 (F and G), IL-6 (H and I), TNF-α (J and K), and IL-1β (L and M) in aortic sinus sections from nicotine-treated ApoE −/− mice ( n = 8; scale bars, 200 μm). (N and O) Immunohistochemical staining and quantification of KLF7 expression in the aortic sinus ( n = 8; scale bars, 200 μm). (P and Q) Representative immunofluorescence images (P) of aortic-root atherosclerotic lesions stained for KLF7 (red), CD68(green; macrophage marker), and DAPI (blue; nuclei), with corresponding quantification of KLF7 fluorescence intensity (Q; n = 8; scale bars, 100 μm). (R) Alterations in body weight of ApoE −/− mice over a 12-week period in NC and miR-210-3p inhibition groups. (S–V) Serum lipid profiles, including TC, TG, LDL-C, and HDL-C, in NC and miR-210-3p inhibition groups ( n = 9). Values are shown as mean ± SEM. Statistical significance was determined using unpaired, two-tailed Student’s t tests. Sample sizes (n) indicate biological replicates per group; each dot represents one biological replicate (individual mouse). ∗p < 0.05 , ∗∗p < 0.01 , ∗∗∗p < 0.001 , ∗∗∗∗p < 0.0001.

Article Snippet: HDL-C assay kit , Nanjing Jiancheng Bioengineering , Cat# A112-1-1.

Techniques: Inhibition, Negative Control, Injection, Staining, Immunohistochemical staining, Expressing, Immunofluorescence, Marker, Fluorescence, Two Tailed Test

Journal: Frontiers in Nutrition

Article Title: Redistribution of branched-chain amino acid intake between active and inactive phases modulates hepatic metabolism in rats

doi: 10.3389/fnut.2026.1754879

Figure Lengend Snippet: Experimental design, growth, intake partitioning, skeletal-muscle S6 signaling, and endpoint plasma markers under phase-shifted BCAA regimens. (A) Simplified study design: rats were maintained on a 12-h light:12-h dark cycle and assigned for 12 weeks to Ctrl (AIN-93G throughout), D + N − (BCAA+20 during the light/inactive phase and BCAA−20 during the dark/active phase), or D − N + (BCAA−20 during the light/inactive phase and BCAA+20 during the dark/active phase), where BCAA+20 and BCAA−20 denote diets containing ~20% higher or lower total BCAA content than Ctrl, respectively; daily energy and nitrogen were intended to be matched while allowing minor day-to-day variation during implementation ( n = 6/group). (B,C) Individual body weight trajectories from week 0 (acclimation) to weeks 1–12 (experimental period) (B) and weekly body weight distributions shown as boxplots (weeks 1–12) with pairwise between-group comparisons annotated above brackets (C) . (D,E) Representative immunoblots of total ribosomal protein S6 and phosphorylated S6 (p-S6, Ser235/236) in skeletal muscle at the end of the study, with total protein staining (TPS; Ponceau S) used for normalization ( n = 4/group; region approximately ~32 kDa displayed) (D) , and densitometric quantification of S6/TPS, p-S6/TPS, and phosphorylation ratio (p-S6/S6 computed as (p-S6/TPS)/(S6/TPS)) with individual animals overlaid (E) . (F) Weekly feed intake partitioned by circadian phase (inactive/light phase: 07:00–19:00; active/dark phase: 19:00–07:00); within each week, upper brackets/ p -values compare whole-day (24 h) total intake between the groups, and lower brackets/ p -values compare inactive vs. active intake within each group (red p-values indicate p < 0.05 as displayed). (G) Endpoint fasting plasma HDL-C, LDL-C, triglycerides (TG), total cholesterol (TC), and malondialdehyde (MDA) across the groups (units as indicated on axes). Group colors follow Ctrl (red), D − N + (green), and D + N − (blue). Boxplots show median and interquartile range (IQR), whiskers extend to 1.5 × IQR, and points indicate individual values (with outliers beyond whiskers where shown). Pairwise statistics were computed using two-sided t-tests with Holm p -value adjustment.

Article Snippet: Specifically, serum lipids were quantified by measuring total cholesterol (TC) using the Total Cholesterol (TC) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K109-M), high-density lipoprotein cholesterol (HDL-C) using the HDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) using the LDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K205-M), malondialdehyde (MDA) using the Malondialdehyde (MDA) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K025-M), and triglycerides (TGs) using the Triglyceride (TG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K261-M).

Techniques: Clinical Proteomics, Western Blot, Staining, Phospho-proteomics