Michael J. Econs, MD

Distinguished Professor

Glenn W. Irwin, Jr. Professor of Endocrinology and Metabolism

Professor of Medicine

Professor of Medical & Molecular Genetics

Division Chief

Address: Gatch Hall, Suite 459
1120 W. Michigan St.
Indianapolis, IN 46202-5111
PubMed:

Bio

Dr. Econs is Distinguished Professor of Medicine and Medical and Molecular Genetics and is the director of the division of Endocrinology and Metabolism. He enjoys mentoring fellows and young faculty. He is particularly proud of the outstanding faculty and fellows that he has recruited and/or mentored over the years.

His own area of interest is metabolic bone disease. In this regard, he sees patients with a variety of bone and mineral disorders and his lab does clinical, translational and basic studies of metabolic bone disease. He teaches fellows, residents and students in his metabolic bone clinic as well as on the general endocrine consult service. Work in the Econs lab led to the discovery of FGF23, which eventually led to the first new therapy in over 30 years for X-linked hypophosphatemic rickets (XLH) and tumor induced osteomalacia (burosumab, Crysvita^®). His past work described novel clinical features of autosomal dominant hypophosphatemic rickets (ADHR), which eventually led to an understanding of the relationship between iron deficiency and increases in FGF23. The IU group recently published a paper demonstrating successful treatment of ADHR with low dose oral iron (Imel et al, JBMR 2020). His lab is currently performing translational studies in autosomal dominant osteopetrosis (ADO2) using a mouse model of this disease, which was developed in his lab, and he and Dr. Imel have initiated a natural history study in ADO2 patients. His lab continues to do research in the genetics of osteoporosis and is performing translational studies of a novel gene.

Default table
Year	Degree	Institution
1989	Fellowship	Duke University Medical Center
1986	Residency	University of Maryland
1983	MD	University of California, San Francisco
1979	BA	Johns Hopkins University

His general area of interest is the genetic aspects of metabolic bone disease. In this regard, He performs clinical, translational and basic studies of metabolic bone disorders. He played critical roles in the discovery of the genes responsible for X-linked hypophosphatemic rickets (PHEX), autosomal dominant hypophosphatemic rickets (FGF23), autosomal dominant osteopetrosis (CLCN7), and osteoglophonic dysplasia (FGFR1). As noted above, his lab’s work in FGF23 led to the first new therapy for XLH and tumor induced osteomalacia in 30+ years and the use of oral iron supplements for the treatment of ADHR. His work also provided proof of concept that unglycosylated FGF23 can be used to treat familial tumoral calcinosis.

Dr. Econs was recruited to Indiana University to bring his program in phosphate homeostasis and lead the genetics of osteoporosis program. Upon arrival, he was asked to see patients having ADO2. Recognizing that there was a high concentration of families with ADO2 locally, he began to study the disorder. His studies eventually led to identification of missense mutations in CLCN7 as the cause of ADO2. Subsequently, his lab found through cell culture studies that the difference between ADO2 carriers and affected individuals was due to differences in the osteoclasts instead of the bone microenvironment (Chu et al JBMR 2006). To study the pathophysiology of the disease further, they made an animal model of ADO2. This model has already allowed them to test multiple therapies and he and Dr. Imel performed a clinical trial using one of these. Along with Dr. Imel, he has initiated an ADO2 natural history study. Once again, his lab used a combination of human studies, mouse models, and cell culture to test clinically and translationally important hypotheses about a human disease.

In addition to the work above, his lab has a major interest in the genetics of osteoporosis. In collaboration with a large international group of investigators, they performed genome-wide association studies for several complex traits. This work led to a landmark publication identifying 56 loci that affect bone mineral density (Estrada et al Nat Genetics 2012), plus several other publications on the genetic determinants of vitamin D status (Wang et al Lancet, 2010) and age of menarche (Perry et al Nature, 2014). His laboratory has taken this work directly into animal models, resulting in creation of the WNT16-overexpressing transgenic mouse (Alam et al, Endocrinology 2015), which has a high bone mass phenotype. Moreover, his unpublished work using allele-specific expression in human bone has identified 4 genes for which expression differences likely play critical roles in the determination of bone density. Cell culture studies have guided them to focus on one of these genes. The KO mouse model has a severe bone phenotype and his lab is exploring mechanisms by which the protein affects bone strength.

Dr. Econs states that he has not limited himself to a particular type of investigation, but instead sought out new approaches and collaborators, because he understands that staying in one’s “comfort zone” limits the significance of the science. Therefore, he uses a wide variety of tools (human studies, mouse models and cell culture) to answer practical questions about a variety of diseases and physiologies.

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Michael J. Econs, MD

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