40% of people with diabetes develop diabetic nephropathy, a leading cause of chronic kidney failure. The research, published in Scientific Reports, demonstrates that the protein RAB27A regulates the non-coding RNA content of extracellular vesicles released by podocytes, cells essential for kidney filtration. It also identifies the microRNA miR-30d-5p as a potential mediator of mechanisms related to kidney damage.
The study, driven by the INCLIVA's Cardiometabolic and Renal Risk Study Group, with participation from Dr. Olga Martínez and PhD candidates Ana Flores and Lesley Escrivá, analyzes how diabetes modifies extracellular vesicles, small particles acting as cellular communication vehicles. These vesicles carry non-coding RNAs, such as microRNAs, which could be involved in diabetic nephropathy.
Diabetes affects millions worldwide, with the kidney being one of the most affected organs. Diabetic nephropathy impairs kidney filtration capacity and is often detected by the presence of proteins in urine (albuminuria). However, this indicator does not always reflect early-stage damage. Therefore, identifying new biomarkers and molecular mechanisms is a key research challenge.
Researchers used an in vitro model of diabetic kidney disease with human podocytes cultured under high glucose conditions. They reduced the expression of the protein RAB27A, essential for vesicular traffic, and analyzed the content of released extracellular vesicles. Results revealed a significant decrease in the microRNA miR-30d-5p, which regulates the expression of SMAD1, a protein involved in kidney fibrosis.
The research also involved Dr. Sergio Martínez Hervás from INCLIVA's Cardiometabolic and Renal Risk Research Group, Dr. María José Forner from the Cardiometabolic and Renal Risk Study Group, and Dr. Josep Redón. Doctors Benedetta Bussolati and Cristina Grange from the University of Turin also collaborated, and the study was conducted within various CIBER research areas.
