DMP1 prevents osteocyte alterations, FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease

Abstract

Therapies based on a bone growth protein could prevent heart failure in chronic kidney disease (CKD) patients, say researchers in the USA. CKD often causes reduced bone mass and leads to left ventricular hypertrophy, a dangerous thickening of heart muscle related to over-production of the FGF23 hormone. In contrast, the dentin matrix protein DMP1, produced by bone cells, is known to reduce FGF23 levels and enhance bone growth. Aline Martin at Northwestern University in Chicago and co-workers increased the DMP1 levels in CKD mouse models through genetic modification and drugs, and found that this treatment restored regular bone mass, lowered FGF23 levels, reduced the occurrence of heart problems and led to longer lives. The findings suggest that therapies that restore DMP1 have the potential to improve both bone and heart health in CKD patients.

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Funding

U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)(R01DK101730)