Raghu G. Mirmira, MD, PhD
Director, Diabetes Research Center
Dr. Raghu Mirmira received his bachelor’s, MD, and PhD degrees from the University of Chicago. Dr. Mirmira subsequently completed his residency in Internal Medicine and subspecialty training in Diabetes and Endocrinology at the University of California at San Francisco. During his fellowship, Dr. Mirmira did his research training in the laboratory of Michael German, where he studied how insulin-producing beta cells form during development in the embryo. Dr. Mirmira then joined the faculty at the University of Virginia, where he studied transcription factors that direct the development and function of beta cells, including Nkx6.1 and Pdx1. His research has more recently focused on mechanisms by which inflammation affects the islet ? cell in type 1 diabetes mellitus. Dr. Mirmira is currently the Eli Lilly Professor in Pediatric Diabetes and Director of the Herman B Wells Center for Pediatric Research, Director of the Center for Diabetes and Metabolic Diseases at Indiana University in Indianapolis, and Director of the MD/PhD (MSTP) program at IU School of Medicine.
Titles & Appointments
- Eli Lilly and Company Professor of Pediatric Diabetes
- Professor of Pediatrics
- Professor of Medicine
- Adjunct Professor of Cellular & Integrative Physiology
- Adjunct Professor of Biochemistry & Molecular Biology
- Director, Center for Diabetes and Metabolic Diseases
- Director, Herman B Wells Center for Pediatric Research
- Director, Medical Scientist Training Program
My research program has centered upon diabetes and the biology of the islet. Four distinct but inter-related research themes have emerged in my research over the years: (1) the biochemical properties of islet-specific transcription factors and the mechanisms by which they regulate islet development and function, (2) the structure and role of islet gene chromatin in the maintenance of islet function, and (3) the integration of extracellular signals (e.g. cytokines, lipids, glucose) with intra-islet death and survival pathways in the setting of diabetes, and (4) identification of biomarkers of β cell stress and death in diabetes. More recently, my research work has focused on islet stress pathways in type 1 diabetes, and how these stress pathways contribute to the production of neoantigens and the activation of autoimmune responses. My laboratory has been interested in the identification of biomarkers of early type 1 diabetes that reflect activation of these stress pathways, including the development of PCR-based techniques for the identification of differentially methylated DNA.
Chronic high fat feeding restricts islet mRNA translation initiation independently of ER stress via DNA damage and p53 activation.
Inhibition of 12/15-Lipoxygenase Protects Against ß-Cell Oxidative Stress and Glycemic Deterioration in Mouse Models of Type 1 Diabetes.
12-Lipoxygenase Inhibitor Improves Functions of Cytokine-Treated Human Islets and Type 2 Diabetic Islets.
Peroxisome Proliferator-activated Receptor-? Activation Augments the ß-Cell Unfolded Protein Response and Rescues Early Glycemic Deterioration and ß Cell Death in Non-obese Diabetic Mice.
IRS1 deficiency protects ß-cells against ER stress-induced apoptosis by modulating sXBP-1 stability and protein translation.
Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet ß Cell Death.
Proinsulin and heat shock protein 90 as biomarkers of beta-cell stress in the early period after onset of type 1 diabetes.
SET7/9 Enzyme Regulates Cytokine-induced Expression of Inducible Nitric-oxide Synthase through Methylation of Lysine 4 at Histone 3 in the Islet ß Cell.
Elevations in Circulating Methylated and Unmethylated Preproinsulin DNA in New-Onset Type 1 Diabetes.
Leukotriene B4-mediated sterile inflammation promotes susceptibility to sepsis in a mouse model of type 1 diabetes.
Transcriptional activity of the islet ß cell factor Pdx1 is augmented by lysine methylation catalyzed by the methyltransferase Set7/9.
Visible light-initiated interfacial thiol-norbornene photopolymerization for forming islet surface conformal coating.
Insulin regulates carboxypeptidase E by modulating translation initiation scaffolding protein eIF4G1 in pancreatic ß cells.
Palmitate induces mRNA translation and increases ER protein load in islet ß-cells via activation of the mammalian target of rapamycin pathway.
Syntaxin 4 up-regulation increases efficiency of insulin release in pancreatic islets from humans with and without type 2 diabetes mellitus.
Lost in translation: endoplasmic reticulum stress and the decline of ß-cell health in diabetes mellitus.
Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains.
Effects of combination therapy with dipeptidyl peptidase-IV and histone deacetylase inhibitors in the non-obese diabetic mouse model of type 1 diabetes.
Protective effects of polyamine depletion in mouse models of type 1 diabetes: implications for therapy.
Mouse islet of Langerhans isolation using a combination of purified collagenase and neutral protease.
Amelioration of type 1 diabetes following treatment of non-obese diabetic mice with INGAP and lisofylline.
Islet ß-cell endoplasmic reticulum stress precedes the onset of type 1 diabetes in the nonobese diabetic mouse model.
The unique hypusine modification of eIF5A promotes islet beta cell inflammation and dysfunction in mice.
Peroxisome proliferator-activated receptor gamma activation restores islet function in diabetic mice through reduction of endoplasmic reticulum stress and maintenance of euchromatin structure.
Liver X receptor agonists augment human islet function through activation of anaplerotic pathways and glycerolipid/free fatty acid cycling.
American Diabetes Association
American Society for Clinical Investigation
American Society for Microbiology
American Board of Internal Medicine - Internal Medicine