Macrophages at the intersection of kidney and cardiovascular disease

Alterations in macrophage function and phenotype have been implicated in complex human diseases. In our work investigating the role of macrophages in APOL1 nephropathy and atherosclerosis, we have discovered that genetic variants driving APOL1-mediated disease induce increased organelle stress and changes in macrophage phenotype. Outside of APOL1-related diseases, we have also detected sex-based differences in macrophage abundance and phenotype in human kidney disease as well as animal kidney injury models. We seek to understand the molecular mechanisms by which organelles modulate macrophage function in the development and progression of kidney and cardiovascular disease.