This review summarizes two decades of research on the pathogenesis of endothelial cell dysfunction in chronic kidney disease, highlighting premature senescence and endothelial-to-mesenchymal transition.
Endothelial senescence and EndMT in CKD merit targeted study; extends pathogenesis synthesis but leaves open therapeutic validation.
Cardiovascular complications dominate the landscape of chronic kidney diseases (CKD). Endothelial cell dysfunction (ECD) is a well-known culprit of cardiovascular morbidity and it develops in CKD with remarkable frequency. This brief overview of ECD in CKD scans two decades of studies performed in my laboratory, from genetic analyses to proteomic and metabolomics screens. I provide a detailed description of findings related to the premature senescence of endothelial cells, cell transition from the endothelial to mesenchymal phenotype, and stages of development of ECD. Clinical utility of some of these findings is illustrated with data on laser-Doppler flowmetry and imaging in patients with CKD. Some currently available and emerging therapeutic options for the management of ECD are briefly presented.
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Michael S. Goligorsky (2015) studied this question.
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