Journal: Aging Cell

Article Title: High‐Fat Diet–Induced Metabolic Stress Durably Reprograms the Liver Regenerative Compartment Toward a Senescence‐Like State

doi: 10.1111/acel.70769

Figure Lengend Snippet: HFD induces aging‐like hepatic dysfunction under chronic metabolic stress. (A) Experimental design. (B) Body weight and caloric intake ( n = 41–44/group). (C) Liver and white adipose tissue (WAT) weights ( n = 9–11/group). (D) Serum total cholesterol (T‐Cho), HDL cholesterol (HDL‐C), non‐HDL cholesterol (non‐HDL‐C), and triglycerides (TG) ( n = 11/group). (E) Representative hematoxylin–eosin (HE) and Oil Red O staining of liver sections. Scale bar, 50 μm. (F) Hepatic TG content and lipid peroxidation (LPO) levels ( n = 6/group). (G) Hepatic inflammatory cytokine levels (IL‐1β, IL‐6, and TNF‐α) ( n = 5/group). (H) Representative images of SA‐β‐gal staining and immunostaining for p16, p21, γH2AX, and Lamin B1 in liver sections. Arrows indicate positive cells. Scale bars, 100 μm. (I) Quantification of the SA‐β‐gal‐positive area, the numbers of p16‐, p21‐, and γH2AX‐positive cells, and Lamin B1 fluorescence intensity ( n = 4–5/group). Data are presented as mean ± SD. Body weight and caloric intake were analyzed using Bonferroni's multiple comparison test. All other data were analyzed using Student's t ‐test. * p < 0.05; ** p < 0.01.

Article Snippet: For immunohistochemistry, sections were incubated with mouse anti‐p16 (1:400; Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti‐p21 (1:2000; Proteintech, Rosemont, IL, USA), mouse anti‐γH2AX (1:2000; Santa Cruz Biotechnology), or rabbit anti‐Ki67 (1:800; Abcam, Cambridge, UK) followed by Histofine Simple Stain MAX‐PO (MULTI) and DAB visualization.

Techniques: Tissue, Staining, Immunostaining, Fluorescence, Comparison

Journal: Aging Cell

Article Title: High‐Fat Diet–Induced Metabolic Stress Durably Reprograms the Liver Regenerative Compartment Toward a Senescence‐Like State

doi: 10.1111/acel.70769

Figure Lengend Snippet: HFD impairs regenerative responses and enhances senescence‐associated changes after CCl 4 ‐induced liver injury. (A) CCl 4 ‐induced liver injury and regeneration model. In this injury context, facultative regenerative programs involving liver stem/progenitor cells have been reported to contribute, at least in part, to epithelial repair. (B) Eight weeks of dietary feeding followed by two CCl 4 injections within 1 week (1 mL/kg body weight diluted 1:1 in olive oil). Regenerating livers were assessed 2 weeks after the final injection. (C) Representative staining images and quantification of the percentage of Ki67‐positive cells in regenerating livers (% nuclei; n = 3–6 per group). (D) Representative staining images of p16, p21, and γH2AX in regenerating liver tissue. Arrows indicate positive cells. Scale bar: 100 μm. (E) Quantification of the percentage of senescence marker‐positive cells in regenerating livers (% nuclei; n = 3–6/group). (F) Temporal changes in the percentages of p16‐, p21‐, and γH2AX‐positive cells before and after CCl 4 injury ( n = 3–6/group). (G) p16‐ and γH2AX‐positive cells among Ki67‐positive cells in regenerating livers ( n = 3–6/group). Data are presented as mean ± SD. * p < 0.05; ** p < 0.01, Student's t ‐test.

Article Snippet: For immunohistochemistry, sections were incubated with mouse anti‐p16 (1:400; Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti‐p21 (1:2000; Proteintech, Rosemont, IL, USA), mouse anti‐γH2AX (1:2000; Santa Cruz Biotechnology), or rabbit anti‐Ki67 (1:800; Abcam, Cambridge, UK) followed by Histofine Simple Stain MAX‐PO (MULTI) and DAB visualization.

Techniques: Injection, Staining, Tissue, Marker, Stem Cell

Journal: Aging Cell

Article Title: High‐Fat Diet–Induced Metabolic Stress Durably Reprograms the Liver Regenerative Compartment Toward a Senescence‐Like State

doi: 10.1111/acel.70769

Figure Lengend Snippet: Liver organoids from HFD‐fed rats exhibit reduced formation capacity and a persistent senescence‐associated phenotype. (A) Liver tissues from control and HFD‐fed rats were dissociated, and regenerative cell–enriched fractions were cultured in Matrigel domes to generate organoids. (B) Representative images of primary organoids. Scale bar, 500 μm. (C) Organoid size distribution and diameter ( n = 6–10/group). (D) Organoids were mechanically disrupted and replated at each passage to assess self‐renewal capacity. (E) Representative images of organoids at Passages 1 (P1), 5, 8, 10, and 13. Scale bar, 200 μm. (F) Organoid formation efficiency during serial passaging. The formation rate is expressed as a percentage of the number of P1 organoids and is normalized to 100% ( n = 6–10/group). (G) Kaplan–Meier survival analysis of organoid formation. Loss of organoid formation was defined as the absence of organoids measuring > 100 μm in diameter ( n = 6–10/group). (H) Representative images of SA‐β‐gal staining and immunofluorescence staining for p16, p21, γH2AX, Ki67, and Lamin B1 in organoid sections at P1–3. DAPI (blue) labels nuclei. Green fluorescence indicates p16, γH2AX, and Lamin B1, whereas red fluorescence indicates p21 and Ki67. Scale bar, 50 μm. (I) Quantification of the SA‐β‐gal‐positive area, the numbers of p16‐, p21‐, γH2AX‐, and Ki67‐positive cells, and Lamin B1 fluorescence intensity at each passage ( n = 4–6/group). (J) Passage‐dependent changes in each senescence‐associated marker ( n = 4–6/group). Each animal‐derived organoid culture was considered one biological replicate. Formation efficiency is presented as mean ± SE; all other data are presented as mean ± SD. Survival curves were analyzed using the Kaplan–Meier method, and statistical significance was determined using the log‐rank test. All other data were analyzed using Student's t ‐test. * p < 0.05; ** p < 0.01.

Article Snippet: For immunohistochemistry, sections were incubated with mouse anti‐p16 (1:400; Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti‐p21 (1:2000; Proteintech, Rosemont, IL, USA), mouse anti‐γH2AX (1:2000; Santa Cruz Biotechnology), or rabbit anti‐Ki67 (1:800; Abcam, Cambridge, UK) followed by Histofine Simple Stain MAX‐PO (MULTI) and DAB visualization.

Techniques: Organoids, Control, Cell Culture, Passaging, Analysis, Staining, Immunofluorescence, Fluorescence, Marker, Derivative Assay

Journal: Frontiers in Oncology

Article Title: GSTP1 as a senescence-associated diagnostic candidate in prostate cancer: integrative bioinformatics and functional validation

doi: 10.3389/fonc.2026.1917548

Figure Lengend Snippet: Key regulatory networks in PCa identified by functional enrichment analysis. (A) Bar plot illustrating significantly enriched Gene Ontology (GO) terms based on DEGs (p < 0.05). (B) Circular plot representing the enriched GO terms (p < 0.05). (C) Bubble plot of enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways (p < 0.05). (D) Network diagram of the enriched KEGG pathways (p < 0.05). (E) Pathview visualization demonstrated systemic activation of PCa pathway.

Article Snippet: After washing with the detergent, add the secondary antibody again: rabbit polyclonal anti-P21 (1:1000 dilution, 10355-1-AP, Proteintech, China), rabbit Polyclonal anti-P16 (1:1000 dilution, 10883-1-AP, Proteintech, China).

Techniques: Functional Assay, Analysis, Activation Assay, Protein-Protein interactions