Vascular calcification contributes centrally to the increased cardiovascular morbidity and mortality in patients with diabetes or chronic kidney disease. Vascular calcification is of major clinical importance as it predicts cardiovascular events, affects plaque stability contributing to stroke and myocardial infarction and also contributes to chronic heart failure by stiffening of the arterial wall. However, the cellular origin of vascular calcification is incompletely understood.
New research led by Dr. Rafael Kramann of the Division of Nephrology and Clinical Immunology shows that adventitial Gli1+ cells are progenitors of vascular smooth muscle cells and participate in acute vascular injury repair. However, during chronic vascular injury as in chronic kidney disease the adventitial progenitor cells maldifferentiate into calcifying vascular cells driving vascular calcification. Genetic ablation of this cell population could completely abolish vascular calcification. The findings published in Cell Stem Cell, will help to develop novel therapeutics for the vast and growing patient population suffering from athero-and arteriosclerosis with vascular calcification.