She was asked to comment on an article in the journal Cell Metabolism titled: “Insulin signaling to the glomerular podocyte is critical for normal kidney function.”
“It is truly an honor to be invited by such a prestigious journal to comment on the work of other scientists in my field who are also working on diabetic related kidney disease,” said Dr. Fornoni, who runs the Diabetic Nephropathy Clinic at the Diabetes Research Institute, where she translates her laboratory research into patient care and brings unanswered clinical questions to the bench.
“Dr. Fornoni has been a rising star among the new generation of Diabetes Research Institute physician scientists since she arrived at the University,” said Camillo Ricordi, M.D., scientific director at the Diabetes Research Institute and chief of the Division of Cellular Transplantation. “I am confident that she will continue to be incredibly productive, contributing to our fight against diabetes and its complications.”
Diabetic nephropathy is a common microvascular complication of diabetes that often results in end-stage renal disease requiring long-term dialysis or kidney transplantation. One of the major focuses of Dr. Fornoni’s research is the identification of the molecular mechanisms responsible for diabetic nephropathy and how those mechanisms can lead to the development of novel therapeutic strategies for prevention and cure.
In her review article titled “Proteinuria, the Podocyte, and Insulin Resistance,” Dr. Fornoni suggests that the ability of the kidney to sense insulin may be one of the key signaling events granting proper function of podocytes, which are the major cellular component of the kidney filtration barrier that is affected in diabetic nephropathy.
“All along we have thought that high glucose and high blood pressure have been the culprits that lead to diabetic nephropathy, but even when you have strict control on these two things, a subset of patients still develop kidney disease, so something else has to be at work,” explains Dr. Fornoni.
“We now know that the kidneys sense insulin in the body and that impaired insulin signaling in podocytes leads to a renal lesion very similar to diabetic nephropathy even in the absence of high glucose. Therefore, targeting insulin signaling in podocytes may represent a new therapeutic strategy to prevent the leakage of protein into the urine and the development of diabetic nephropathy.”
Dr. Fornoni has published 40 peer-reviewed articles in various journals over the past eight years.
“To take the complex disease signaling in diabetes apart and track down the essence of what causes renal disease in diabetes is at the core of what Dr. Fornoni does, and this comes through clearly in her thoughtful editorial,” said Jochen Reiser, M.D., Ph.D., professor and chief of the Division of Nephrology and Hypertension and vice chair for research in the Department of Medicine.