Treatment with the senolytic ABT-263 allows recovery of HPC mitochondrial health in aged BM. Aged C57Bl/6 mice were treated with 100 mg/kg ABT-263 or vehicle control for 7 days followed by treatment with 0.4 mg/kg LPS or vehicle control. They were killed after 12 hours and their BM isolated. (A) MSC frequency in ABT-263–treated aged mice compared with age-matched control mice. (B) MSCs were FACS-purified, and gene expression of p16 was measured by using RT-qPCR, relative to glyceraldehyde-3-phosphate dehydrogenase, in aged mice treated with ABT-263 or vehicle control. (C) Cell number of LSKs, LS-Ks, and MPPs in aged control mice and ABT-263–treated mice with or without LPS treatment. (D) Flow cytometry was used to measure the frequency of TMRM^hi LSKs, LS-Ks, and MPPs after LPS treatment in ABT-263–treated C57Bl/6 mice and age-matched control mice. (E) Changes in basal and maximal respiration measured by Seahorse metabolic flux analysis. (F) Biolog analysis of glycolytic and TCA cycle substrates in aged mice and ABT-263–treated aged mice after LPS treatment compared with control mice. Not detected (ND) levels are labeled, and 1 represents no change. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P < .0001 using the Mann-Whitney U test or two-way analysis of variance. Con, vehicle control; ns, not significant.