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Anna Mae Diehl

Florence McAlister Distinguished Professor of Medicine
Medicine, Gastroenterology
Duke Box 3256, 905 S. LaSalle Street, GSRB 1, Durham, NC 27710
Ste 1073, GSRB 1, 595 LaSalle Street, Durham, NC 27710

Overview


Our lab has a long standing interest in liver injury and repair. To learn more about the mechanisms that regulate this process, we study cultured cells, animal models of acute and chronic liver damage and samples from patients with various types of liver disease. Our group also conducts clinical trials in patients with chronic liver disease. We are particularly interested in fatty liver diseases, such as alcoholic fatty liver disease and nonalcoholic fatty liver disease (NAFLD).

Research by our group has advanced understanding in two main areas: 1) immune system regulation of liver injury and regeneration and 2)the role of fetal morphogens, such as the hedgehog pathway, in regulating fibrotic responses to liver damage. Our basic research programs have been enjoyed continuous NIH support since 1989. We welcome students, post-doctoral fellows and visiting scientists who have interests in this research area to contact us about training opportunities and potential collaborations.

Since 2001 we have also been an active participant in the NIDDK-funded Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN), a national consortium comprised of 8 university medical centers selected to generate a national registry for patients with NAFLD and to conduct multicenter treatment trials for this disorder. We are actively recruiting patients for this program, as well as a number of other industry-supported NAFLD studies.

Current Appointments & Affiliations


Florence McAlister Distinguished Professor of Medicine · 2005 - Present Medicine, Gastroenterology, Medicine
Professor of Medicine · 2004 - Present Medicine, Gastroenterology, Medicine
Member of the Duke Cancer Institute · 2004 - Present Duke Cancer Institute, Institutes and Centers
Affiliate of the Duke Regeneration Center · 2021 - Present Duke Regeneration Center, Basic Science Departments

In the News


Published July 1, 2024
Liver Damage from Stress and Aging Might Be Reversible
Published October 29, 2018
Our Microbes Are Starving, and That’s a Good Thing

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Recent Publications


Bile salt hydrolase activity as a rational target for MASLD therapy.

Journal Article Gut Microbes · December 31, 2026 Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease in the United States, yet therapeutic options remain limited. Emerging evidence implicates the gut‒liver axis and intestinal permeability in diseas ... Full text Link to item Cite

Zinc-dependent RNA-binding protein controls hepatocyte senescence and recovery from alcohol-related liver failure.

Journal Article Gut · January 13, 2026 BACKGROUND: Why alcohol-associated liver disease (ALD) resolves after abstinence in most people but progresses to liver failure in others remains poorly understood. Experimental models show that increased exposure to proinflammatory cytokines exacerbates A ... Full text Link to item Cite

Association of Components of Metabolic Syndrome and the Progression of Nonalcoholic Fatty Liver Disease.

Journal Article Am J Gastroenterol · January 1, 2026 INTRODUCTION: The effects of metabolic syndrome (MetS), its individual components, and baseline liver histology, on the rates of progression and regression of nonalcoholic fatty liver disease (NAFLD), were evaluated. METHODS: We conducted a post hoc analys ... Full text Link to item Cite
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Recent Grants


2/3 CTSA K12 Program at Duke University

ResearchMentor · Awarded by National Institutes of Health · 2025 - 2030

TNF alpha and Recovery from Alcoholic Liver Injury

ResearchPrincipal Investigator · Awarded by National Institutes of Health · 2014 - 2030

Targeting Hepatocyte Senescence to Improve NAFLD

ResearchMentor · Awarded by National Institute of Diabetes and Digestive and Kidney Diseases · 2024 - 2029

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Education, Training & Certifications


Georgetown University · 1978 M.D.