Carmella Evans-Molina, MD, PhD
J. O. Ritchey Scholar in Medicine
Dr. Evans-Molina’s research program is focused on defining the molecular and inflammatory etiologies of β-cell dysfunction that contribute to the pathophysiology of diabetes mellitus. Her lab has several ongoing laboratory-based projects focused on:
1. Understanding the pathways that regulate intracellular calcium homeostasis in the pancreatic β-cell endoplasmic reticulum, Golgi apparatus, and secretory granules;
2. Defining the role of intracellular calcium dyshomeostasis during the evolution of Type 1 and Type 2 diabetes;
3. The development and implementation of novel imaging techniques to monitor β-cell calcium flux under conditions of health and disease; and
4. Elucidating pathways that lead to macrophage activation and islet infiltration in Type 1 and Type 2 diabetes.
In addition, Dr. Evans-Molina’s lab has ongoing translational and clinical projects focused on the discovery and validation of novel serum biomarkers that identify early β cell-stress in clinically silent Type 1 diabetes, with the goal of applying these biomarkers in diabetes prevention paradigms or as surrogate clinical endpoints in response to therapeutic interventions. She is an investigator in the Type 1 Diabetes TrialNet Clinical Network, where she serves as as a Scientific Advisor, Chair of the β-Cell and Metabolism Working Group, and.Chair of the Long-Term Investigative Follow-Up (LIFT) study. Dr. Evans-Molina is also a member of the NIH Human Islet Research Network, where she serves as Chair of the Translational Working Group. Her research is supported by grants from the NIH, JDRF, and the VA.
Dr. Evans-Molina earned her M.D. degree from Marshall University in Huntington, WV and completed her residency training in Internal Medicine at the Massachusetts General Hospital in Boston, MA. She completed her subspecialty training in Endocrinology and Metabolism at the University of Virginia in Charlottesville, VA. In parallel with this phase of her clinical training, Dr. Evans-Molina earned a Ph.D. in Pharmacology, also from the University of Virginia. She joined the faculty of the Indiana University School of Medicine in 2008. Dr. Evans-Molina is the J.O. Ritchey Scholar in Medicine and has been named an IU School of Medicine Showalter Scholar. She is an Associate Professor in the Department of Medicine and holds joint appointments in the Departments of Cellular and Integrative Physiology, Biochemistry and Molecular Biology and the Herman B. Wells Center for Pediatric Research. She currently serves as an Associate Director of Development and Community Engagement for the Indiana University Center for Diabetes and Metabolic Diseases (CDMD) and Director of CDMD Islet and Physiology Core. Dr. Evans-Molina is an editorial board member for the journals Translational Research and Endocrinology .
VanNuys Med Sci Bldg, Suite 2031 A 635 Barnhill Dr
Indianapolis, IN 46202-5120
Titles & Appointments
- Associate Professor of Medicine
- Adjunct Associate Professor of Cellular & Integrative Physiology
- Adjunct Associate Professor of Biochemistry & Molecular Biology
- Director of Diabetes Research in the Herman B Wells Center for Pediatric Research
Inflammatory stress of pancreatic beta cells drives release of extracellular heat-shock protein 90a.
Chronic high fat feeding restricts islet mRNA translation initiation independently of ER stress via DNA damage and p53 activation.
STEAP4 expression in human islets is associated with differences in body mass index, sex, HbA1c, and inflammation.
Metabolic dysfunction and adipose tissue macrophages: is there more to glean from studying the lean?: Comment on "Adipose tissue infiltration in normal-weight subjects and its impact on metabolic function" by Moreno-Indias etáal.
The relationship between BMI and insulin resistance and progression from single to multiple autoantibody positivity and type 1 diabetes among TrialNet Pathway to Prevention participants.
HLA-DRB1*15:01-DQA1*01:02-DQB1*06:02 Haplotype Protects Autoantibody-Positive Relatives From Type 1 Diabetes Throughout the Stages of Disease Progression.
A case of extragastrointestinal stromal tumor complicated by severe hypoglycemia: a unique presentation of a rare tumor.
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 ▀ Cell.
Nitric oxide stress and activation of AMP-activated protein kinase impair ▀-cell sarcoendoplasmic reticulum calcium ATPase 2b activity and protein stability.
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.
CD40 promotes MHC class II expression on adipose tissue macrophages and regulates adipose tissue CD4+ T cells with obesity.
Pancreatic and duodenal homeobox protein 1 (Pdx-1) maintains endoplasmic reticulum calcium levels through transcriptional regulation of sarco-endoplasmic reticulum calcium ATPase 2b (SERCA2b) in the islet ▀ cell.
Fetal hyperglycemia and a high-fat diet contribute to aberrant glucose tolerance and hematopoiesis in adult rats.
Palmitate induces mRNA translation and increases ER protein load in islet ▀-cells via activation of the mammalian target of rapamycin pathway.
Shock wave lithotripsy targeting of the kidney and pancreas does not increase the severity of metabolic syndrome in a porcine model.
Human adipose-derived stromal/stem cells protect against STZ-induced hyperglycemia: analysis of hASC-derived paracrine effectors.
Lost in translation: endoplasmic reticulum stress and the decline of ▀-cell health in diabetes mellitus.
Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains.
Urinary biomarkers for the early diagnosis of retinopathy and nephropathy in type 1 diabetes mellitus: a "steady stream" of information using proteomics.
PPAR-? activation restores pancreatic islet SERCA2 levels and prevents ▀-cell dysfunction under conditions of hyperglycemic and cytokine stress.
Islet ▀-cell endoplasmic reticulum stress precedes the onset of type 1 diabetes in the nonobese diabetic mouse model.
The role of peroxisome proliferator-activated receptor ? in pancreatic ▀ cell function and survival: therapeutic implications for the treatment of type 2 diabetes mellitus.
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 Board of Internal Medicine - Internal Medicine