Reena Rao, MPhil, PhD
Professor, Nephrology and Hypertension
Deputy Director, Deputy Director, Jared Grantham Kidney Institute
rrao@kumc.eduMore:
Professional Background
Professor
Dr. Reena Rao is a Professor of Medicine in the Division of Nephrology and Hypertension at the University of Kansas Medical Center, the Deputy Director of the Jared Grantham Kidney Institute, and a Research Scientist at the Kansas City VA Medical Center. Dr. Rao’s research focuses on understanding the mechanisms that drive cyst growth, renal dysfunction, and progressive kidney disease in autosomal dominant polycystic kidney disease (ADPKD), with the goal of developing new therapeutic strategies for patients with polycystic kidney disease.Dr. Rao received her Ph.D. from the Central Food Technological Research Institute in India and completed her postdoctoral fellowship at Vanderbilt University Medical Center before joining the University of Kansas Medical Center. At KUMC, she leads a multidisciplinary research program that integrates genetically engineered mouse models, renal physiology, molecular biology, imaging, and translational studies using human ADPKD cells.Through her research and leadership at the Jared Grantham Kidney Institute, Dr. Rao is committed to advancing collaborative, mechanism-based research in PKD and to training the next generation of kidney disease researchers.
Education and Training
- BSc, Zoology, Catholicate College, Mahatma -Gandhi University, India, Kerala, India
- MSC, Medical Entomology, Vector Control Research Center, Pondicherry, India, Pondicherry, Karnataka
- MPHIL, Zoology, Kerala University, Thiruvanamthapuram, India, Thiruvanamthapuram, Kerala
- PhD, Biotechnology, Central Food Technological Research Institute, Mysore, India, Mysore, Karnataka
- Post Doctoral Fellowship, Nephrology, Vanderbilt University, Nashville, TN, Nashville, TN
Professional Affiliations
- American Heart Association, Member, 2016 - Present
- American Society of Nephrology, Member, 2006 - Present
Research
Overview
Research Focus:
Our research program seeks to understand the mechanisms that drive cyst growth, renal tubular dysfunction, fibrosis, and progressive loss of kidney function in autosomal dominant polycystic kidney disease (ADPKD). We are particularly interested in how tubular epithelial cells respond to their environment and how alterations in epithelial signaling, transport, metabolism, and communication with surrounding stromal cells contribute to disease progression.
Using complementary genetic mouse models, in vivo renal functional studies, imaging, and molecular approaches, our laboratory has defined how signaling pathways, including glycogen synthase kinase-3 and vasopressin signaling, regulate tubular epithelial homeostasis, injury responses, and cyst growth. Our studies have revealed important connections between abnormal epithelial signaling, metabolic dysfunction, tubular injury, and the development of fibrosis in ADPKD.
Our current research is focused on the cyst microenvironment and stroma - epithelial crosstalk. We are investigating how fibroblasts and myofibroblasts interact with cystic epithelial cells and how these interactions promote cyst growth and disease progression. In parallel, we have identified disruption of the renal circadian clock as a previously unrecognized contributor to cyst growth in ADPKD and are investigating whether chronotherapy can be used to slow disease progression.
Our laboratory combines complementary orthologous ADPKD mouse models with renal functional assays and translational studies using primary human ADPKD epithelial cells and fibroblasts. By integrating epithelial, stromal, metabolic, and physiological approaches, we aim to uncover new mechanisms of ADPKD progression and identify therapeutic strategies that can preserve kidney function.
Our ultimate goal is to translate mechanistic discoveries into treatments that slow or prevent disease progression, and, ultimately, to find a cure for polycystic kidney disease.
Selected Publications
- Jamadar Abeda, Remadevi Viji, Ding Wen-XIng, Haase Volker, Rao Reena . 2026. Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease. Cell Commun Signal
- Jamadar Abeda, Ward Christopher, Remadevi Viji, Varghese Meekha, Pabla Navjot, Gumz Michelle, Rao Reena. 2025. Circadian clock disruption and growth of kidney cysts in autosomal dominant polycystic kidney disease.. Journal Of American Society of Nephrology. https://pubmed.ncbi.nlm.nih.gov/39401086/
- Dwivedi N, Tao S, Jamadar A, Sinha S, Howard C, Wallace D, Fields TA, Leask A, Calvet J, Rao R. 2020. Epithelial Vasopressin Type-2 Receptors Regulate Myofibroblast Activation by a YAP Dependent Mechanism in Polycystic Kidney Disease.. Journal of American Society of Nephrology, Aug;31(8):, 1697-1710
- Tao S, Kakade VR, Woodgett JR, Pandey P, Suderman ED, Rajagopal M, Rao R. 2015. Glycogen synthase kinase-3β promotes cyst expansion in polycystic kidney disease.. Kidney international, 87 (6), 1164-75
- Dwivedi N, Jamadar A, Fields T, Rao R. 2023. Myofibroblast depletion reduces kidney cyst growth and fibrosis in autosomal dominant polycystic kidney disease.. Kidney International. , 103 (1), 144-155 . https://pubmed.ncbi.nlm.nih.gov/36273656/
- Remadevi Viji, Jamadar Abeda, Yang Haichun, Gunewardena Sumedha , Wallace Darren, Rao Reena. 2026. Pirfenidone treatment attenuates fibrosis in autosomal dominant polycystic kidney disease. . JCI Insights
- Jamadar A, Suma SM, Mathew S, Fields T, Wallace D, Calvet J, Rao R. 2021. The tyrosine-kinase inhibitor Nintedanib ameliorates autosomal-dominant polycystic kidney disease. Cell Death and Diseases, 2021 October; 12(947), Open Access - No page numbers