Fig 1.
Alterations in renal tubular morphology and renal interstitial collagen deposition were observed in aged mice.
(A) Visual changes of the kidneys of the experimental cohort. (B) Morphological assessment of kidney slices subjected to H&E staining (10×). (C) Masson’s trichrome staining was employed at 10× magnification to detect collagen fibers. (D) Quantitative analysis of the percentage of renal tubular atrophy. (E) Quantitative analysis of the relative density of positive areas in renal tubules, indicating changes in collagen deposition. Data are displayed with the mean ± SEM, with distinct letters (a–b) indicating statistically significant variations (P < 0.05) compared with 12 W. Tubular atrophy and collagen deposition are highlighted by green and yellow arrows, respectively.
Fig 2.
Aging enhances α-SMA expression and collagen accumulation in the kidney.
(A) The expression of α-SMA in renal tubules at 20× magnification. (B) Quantitative analysis of the relative expression of α-SMA in renal tubules. (C) Quantitative analysis of Hydroxyproline content within kidney tissue. (D) The mRNA abundance of the COL1A1 and MMP9 genes within kidney tissue. Data are displayed with the mean ± SEM, with distinct letters (a–b) indicating statistically significant variations (P < 0.05) compared with the findings in the 12 W group.
Fig 3.
Effect of aging on cellular senescence in the mouse kidney.
(A) SA-β-gal staining (displayed in turquoise blue) of kidney slices from mice of varying ages is presented at 20× magnification. (B) The mean density of SA-β-Gal within the renal cortex. (C) Quantitative real-time PCR analysis of the mRNA levels of the aging-associated genes P21 and P53 in the kidney. Data are displayed with the mean ± SEM, with distinct letters (a–b) indicating statistically significant variations (P < 0.05) compared with the findings in the 12 W group.
Fig 4.
Aging impairs renal mitochondrial function and antioxidant capacity.
(A) Representative transmission electron microscopy images of kidney tissue at 10,000× and 20,000× magnification. (B) Quantitative real-time PCR analysis of the antioxidant-associated genes SOD1 and SOD2. Data are displayed with the mean ± SEM, with distinct letters (a–b) indicating statistically significant variations (P < 0.05) compared with the observations in the 12 W group (P < 0.05).
Fig 5.
Aging regulates mRNA levels of renal fibrosis-related genes in mice across varying age cohort.
(A) Changes in mRNA levels of genes associated with profibrosis in 12 W, 32 W, and 43 W mice. (B) Changes in mRNA levels of genes associated with antifibrosis activity in 12 W, 32 W, and 43 W mice. (C) Changes in mRNA levels of genes associated with inflammation in 12 W, 32 W, and 43 W mice. Data are displayed with the mean ± SEM, with distinct letters (a–b) indicating statistically significant variations (P < 0.05) compared with those observed in the 12 W group (P < 0.05).