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Mice were treated with CDDP and NMN as per , and serum collected at 10 weeks of age for measurements of the renal function markers A) blood urea nitrogen (BUN) and <t>B)</t> <t>cystatin</t> C. Renal damage that can impact the excretion of C) phosphate (PO 4 ), which was not altered by these treatments, in contrast to D) elemental phosphorus, which encompasses both soluble, free phosphate, insoluble calcium phosphate precipitates, and organic phosphorus, such as phospholipids. Phosphate homeostasis can be regulated by the bone-derived hormone E) FGF23 and its coreceptor F) <t>Klotho.</t> These also regulate the production of G) parathyroid hormone (PTH), which maintain H) serum calcium levels and promote bone loss through the mobilisation of calcium from bone mineral stores. N=5-6 per group as indicated by data points, p-values are from Bonferroni-adjusted t-tests derived from estimated marginal means of linear model of NMN and CDDP treatment, with results of linear models indicated on each panel
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Mice were treated with CDDP and NMN as per , and serum collected at 10 weeks of age for measurements of the renal function markers A) blood urea nitrogen (BUN) and B) cystatin C. Renal damage that can impact the excretion of C) phosphate (PO 4 ), which was not altered by these treatments, in contrast to D) elemental phosphorus, which encompasses both soluble, free phosphate, insoluble calcium phosphate precipitates, and organic phosphorus, such as phospholipids. Phosphate homeostasis can be regulated by the bone-derived hormone E) FGF23 and its coreceptor F) Klotho. These also regulate the production of G) parathyroid hormone (PTH), which maintain H) serum calcium levels and promote bone loss through the mobilisation of calcium from bone mineral stores. N=5-6 per group as indicated by data points, p-values are from Bonferroni-adjusted t-tests derived from estimated marginal means of linear model of NMN and CDDP treatment, with results of linear models indicated on each panel

Journal: bioRxiv

Article Title: Chemotherapy accelerated bone ageing is reversed by NMN

doi: 10.1101/2025.10.13.679926

Figure Lengend Snippet: Mice were treated with CDDP and NMN as per , and serum collected at 10 weeks of age for measurements of the renal function markers A) blood urea nitrogen (BUN) and B) cystatin C. Renal damage that can impact the excretion of C) phosphate (PO 4 ), which was not altered by these treatments, in contrast to D) elemental phosphorus, which encompasses both soluble, free phosphate, insoluble calcium phosphate precipitates, and organic phosphorus, such as phospholipids. Phosphate homeostasis can be regulated by the bone-derived hormone E) FGF23 and its coreceptor F) Klotho. These also regulate the production of G) parathyroid hormone (PTH), which maintain H) serum calcium levels and promote bone loss through the mobilisation of calcium from bone mineral stores. N=5-6 per group as indicated by data points, p-values are from Bonferroni-adjusted t-tests derived from estimated marginal means of linear model of NMN and CDDP treatment, with results of linear models indicated on each panel

Article Snippet: ELISA kits were used to measure cystatin C (Invitrogen EMCST3), Klotho (Cusabio CSB-E14362m) and FGF23 (Abcam ab213863).

Techniques: Derivative Assay