In conclusion, our data indicate that <i>Hyp</i> mice, in contrast to <i>kl/kl</i> mice appear to be protected from pathological cardiac remodeling during conditions of high FGF23 levels and klotho deficiency, which may be due, at least in part, to differences in mineral metabolism alterations, i.e., hypophosphatemia and lack of hypercalcemia.
The mRNA of STCs is upregulated in the kidney of α-klotho mutant (kl/kl) mice, which have hypercalcemia, hyperphosphatemia and hypervitaminosis D and exhibit a short life span, osteopenia and ectopic calcification.
Recent studies have shown that Klotho mice and Fgf23 mice exhibit identical phenotypes including hyperphosphatemia and hypercalcemia in addition to the aging-like syndrome.