Cardiovascular events, including vascular calcification and uremic cardiomyopathy, account for most deaths in cases of chronic kidney disease/end stage renal disease (CKD/ESRD).
Efficient therapies for cardiovascular events are urgently required to save the lives of patients with CKD/ESRD. Unfortunately, there is slow progress in this field.
Our animal studies have clearly indicated that Klotho protein could reduce vascular calcification and pathologic cardiac remodeling in CKD models. Klotho can also suppress mineralization in cultured vascular smooth muscle cells, as well as inhibit fibrogenesis in cultured cardiac fibroblasts.
These results suggest that Klotho might protect the vasculature and heart against uremic environments, including hyperphosphatemia, through multiple yet-to-be-determined mechanisms.
Klotho has been shown to be deficient in acute kidney injury (AKI). Klotho deficiency is associated with AKI progression to CKD and extra renal complications development in CKD. The role of Klotho in clinical nephrology is of great interest for the future of medicine, today.
During AKI progression to CKD, cardiac function monitored by MRI is dramatically deteriorated (left). Klotho protein administration can efficiently mitigate this deterioration and improves cardiac function of CKD mouse (right).