Alla Mitrofanova, PhD
Assistant Professor,
University of Miami, Peggy and Harold Katz Family Drug Discovery Center
Featured in the Session: Unexplored Pathways of Residual Risk in Diabetic Kidney Disease to Find Novel Cures
When
Sunday, June 7
at 4:30 p.m. CT
Where
R07 (Level 2)
Ernest N. Morial Convention Center
What is your presentation about?
My presentation will focus on how diabetes alters key metabolic and stress-response pathways in podocytes, the specialized cells that help maintain the kidney filtration barrier. I will discuss our studies on sphingolipid metabolism, innate immune signaling, and TFAM-dependent mitochondrial regulation, and how these pathways may interact to promote podocyte injury and diabetes-related kidney disease progression. The goal is to show how podocyte metabolism is not only disrupted in disease, but may also reveal new molecular targets for intervention.
How do you hope your presentation will impact diabetes research or care?
I hope this presentation will encourage researchers to think about diabetes-related kidney disease as a disorder driven not only by systemic metabolic stress, but also by kidney-intrinsic changes within podocytes. By identifying pathways such as sphingolipid remodeling, innate immune activation, and mitochondrial dysfunction, our work may help uncover new therapeutic strategies to protect podocytes before irreversible kidney damage occurs. Ultimately, this could support the development of more targeted treatments for patients with diabetes who are at risk for kidney disease progression.
How did you become involved with this area of diabetes research or care?
I became involved in this area through my long-standing interest in kidney disease, which later on brought me to study the podocyte biology and the mechanisms that drive glomerular injury. As our studies progressed, it became clear that metabolic dysfunction, mitochondrial stress, and inflammatory signaling are closely connected in diabetes-related kidney disease. This led my current research to focus on how podocytes respond to diabetes-related stress and how these responses can be redirected toward protection rather than injury.