María Dolores Sánchez Niño

March 25, 2024

PhD in Biomedicine (UAM) and Master's in Bioinformatics (CNIO-ISCIII). She has conducted research stays at Cancer Research UK, the University of Michigan, and Mount Sinai School of Medicine (USA). In 2015, she received a Miguel Servet grant within the IIS-FJD, where she currently leads her own research line in renal pathology. Since 2020, she has held a Ramón y Cajal contract (MICIIN) in the Department of Pharmacology (UAM). Over recent years, she has been the Principal Investigator (PI) of five competitive research projects (ISCIII), and she is currently the PI of a European H2020-MSCA-ITN-2019 project. She has supervised 10 doctoral theses and 18 undergraduate/master's theses. She holds 7 granted patents and nearly 200 indexed publications. She has delivered numerous lectures at national and international conferences and is involved in teaching Master's and Bachelor's degrees at the Faculty of Medicine (UAM) and the ONCE University School of Physiotherapy, teaching Pharmacology.

Her research line on new therapeutic targets in renal disease and biomarkers for staging and monitoring therapeutic response has gained national and international recognition: 2023 Award for Research Excellence in Nephrology (European Renal Association) and national awards such as the 2021 Young Investigator Award-SEBBM, 2020 Young Researchers-AstraZeneca Award, 2020 Conde de Cartagena-RANME Award, 2020 Leonardo BBVA Fellowship, and the 2017 Iñigo Alvarez de Toledo Basic Nephrology Research Award.

Project Summary and Clinical Relevance

Title: Growth differentiation factor-15 preserves Klotho expression in acute kidney injury and kidney fibrosis. Journal: Kidney International.

Chronic kidney disease (CKD) is expected to become the 5th leading cause of death by 2040, highlighting the scarcity of therapeutic alternatives. CKD promotes the development of acute kidney injury (AKI), and AKI accelerates CKD. Based on an unbiased systems biology approach, a new concept has been explored: the insufficient activation of adaptive factors that protect the kidney during kidney disease. Specifically, GDF15 has been identified as a soluble factor that increases during human and experimental kidney damage but has a protective function in kidney models of AKI and CKD. Initially, genetically modified mice lacking or overexpressing GDF15 were studied. To identify viable clinical treatment alternatives, recombinant GDF15 was also tested, showing protective effects on the kidneys. Ultimately, it was demonstrated that GDF15 is part of an adaptive kidney damage response system, and its protective effect is due to its preservation of Klotho protein production, which has anti-aging properties and protects organs and tissues.