Fig. 5: SSK1 attenuates the SASP and aging-associated signatures in aged mice. | Cell Research

Fig. 5: SSK1 attenuates the SASP and aging-associated signatures in aged mice.

From: Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice

Fig. 5: SSK1 attenuates the SASP and aging-associated signatures in aged mice.

a, b Heatmaps of senescence-related gene expression of livers (a) and kidneys (b) treated with vehicle or SSK1 (0.5 mg/kg). c, d GSEA results of the statistically significant gene set: Hallmark Inflammatory Response. Left: Gene sets enriched in the livers (c) and kidneys (d) from old mice compared with young mice. Right: Gene sets down-regulated in the livers (c) and kidneys (d) of old mice treated with SSK1 compared with vehicle. e–h IL1α (e), IL6 (f), CXCL1 (g), and TNFα (h) protein levels in blood serum from old mice treated with vehicle or SSK1 measured by ELISA. i GSEA of a statistically significant gene set: Kyng Werner Syndyom and Normal Aging Up of livers down-regulated in the old mice treated with SSK1 compared with vehicle. j GSEA of a statistically significant gene set: Rodwell Aging Kidney Up of kidneys down-regulated in the old mice treated with SSK1 compared with vehicle. For (a), (c), and (i): vehicle-treated, n = 5; SSK1-treated, n = 4. For (b), (d), and (j): vehicle-treated, n = 5; SSK1-treated, n = 5. For (e–g): vehicle-treated, n = 5, SSK1-treated, n = 6. For (h): vehicle-treated, n = 7; SSK1-treated, n = 8. Each data point represents an individual mouse. ‘n’ represents the number of mice. Data are presented as means ± SEM. Unpaired two-tailed t-test, *P < 0.05, **P < 0.01.

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