About

Sharon DeMorrow, Ph.D., FAASLD, is a Professor of Pharmacology & Toxicology at the University of Texas at Austin. Her research program broadly focuses on the neurological changes associated with either acute liver failure or chronic liver disorders. These alterations range from changes in neuropeptide hormone expression to severe cognitive impairment and hepatic coma, known as hepatic encephalopathy. Her ongoing studies aim to determine the signaling molecules released from an impaired liver that may alter brain function. Her work is dedicated to understanding the complex interactions between liver dysfunction and brain health, contributing to the fields of pharmaceutical sciences and neurogastroenterology. She is committed to providing exemplary education, training, research, and professional development in the pharmaceutical sciences, with a focus on advancing discovery, innovation, and patient care. Her efforts also include serving the university, professional and scientific communities, and society at large.

Research topics

• Biology
• Intensive care medicine
• Internal medicine
• Bioinformatics
• Pathology
• Biochemistry
• Medicine
• Gastroenterology

Selected publications

• Central administration of recombinant IGF1 is neuroprotective in a rodent model of acute liver failure

  Figshare · 2026-03-30

  datasetOpen accessSenior author

  This dataset contains the raw and processed data supporting the findings of this study. Data are organized by figure panels (Figures 1-8 and Figure S1-2) to facilitate direct comparison with the manuscript. Each folder includes raw data, processed data, and source data used for statistical analysis and figure generation.

  PublisherDOI

• Central Administration of Recombinant IGF1 Is Neuroprotective in a Rodent Model of Acute Liver Failure

  International Journal of Molecular Sciences · 2026-04-16

  articleOpen accessSenior authorCorresponding

  Acute liver failure is often accompanied by neurological disturbances collectively referred to as hepatic encephalopathy (HE), characterized by neuroinflammation and subsequent cognitive decline. Insulin-like growth factor 1 (IGF1) is a neuroprotective peptide with anti-inflammatory properties in the brain. The role of IGF1 in cognitive deficits and neuroinflammation during HE remains largely unexplored. In C57Bl/6 mice, HE was established through an intraperitoneal injection of azoxymethane (AOM), and tissues were collected at defined time points during disease development. IGF1 expression in the cortex was downregulated following AOM administration. Central infusion of recombinant mouse IGF1 (rmIGF1) before AOM injection resulted in delayed neurological impairment, reduced microglial activation, and decreased proinflammatory cytokine and chemokine production in AOM mice. In vitro, rmIGF1 and conditioned media derived from rmIGF1-treated primary neurons attenuated phagocytic activity and C-C motif chemokine ligand 2 (CCL2) production in the microglial cell line EOC-20. Collectively, our results show that IGF1, whose levels decline during HE, alleviates neuroinflammation and improves the pathological state of AOM-treated mice through the suppression of microglial activation and the regulation of neuron-microglia paracrine communication.

  PublisherOA PDFDOI

• Biochemical and Physiological Effects of Galanin in Health and Disease

  The FASEB Journal · 2026-01-17

  articleOpen accessSenior authorCorresponding

  Galanin is a biologically active peptide discovered in 1983 from the intestines of pigs. Discovered by Doctors Tatemoto, Rökaeus, Jörnvall, McDonald, and Mutt, it was found to contract smooth muscle tissue in rat intestine and produce hyperglycemia in dogs. Since its discovery, research into galanin has revealed a wide array of effects in numerous organ systems. As these effects have been uncovered, there has been growing interest in the galanin system as a therapeutic target. Targeting galanin has proven difficult as it influences much of the body, leading to challenges in identifying the source of observed changes and, moreover, selecting those sources as targets. A critical tool in overcoming these challenges is a cohesive understanding of galanin's broad effects in various organ systems. Galanin and galanin receptor expression, receptor and ligand affinity, biochemical signaling paths, and physiological effects of galanin remain under investigation. As research into this field continues, greater appreciation of the complexity of galanergic signaling is critical to elucidate galanin's role in health. This review seeks to provide insight into these aspects and provide researchers with the knowledge needed to continue to expand investigations in the galanergic system.

  PublisherOA PDFDOI

• Central administration of recombinant IGF1 is neuroprotective in a rodent model of acute liver failure

  Figshare · 2026-03-30

  datasetOpen accessSenior author

  This dataset contains the raw and processed data supporting the findings of this study. Data are organized by figure panels (Figures 1-8 and Figure S1-2) to facilitate direct comparison with the manuscript. Each folder includes raw data, processed data, and source data used for statistical analysis and figure generation.

  PublisherDOI

• Characterization of hepatic pathology during azoxymethane-induced acute liver failure

  World Journal of Gastroenterology · 2025-03-26 · 1 citations

  articleOpen access

  BACKGROUND: Acute liver failure (ALF) is a loss of liver function due to a severe hepatic insult. Studies utilizing the azoxymethane (AOM) mouse model of ALF, which also generates hepatic encephalopathy, have primarily focused on development of neurological deficits. However, the molecular processes that generate liver damage have not been fully characterized. Therefore, a more comprehensive characterization of the hepatic consequences of AOM toxicity is needed to better understand this disease model. AIM: To identify molecular pathology contributing to hepatic injury during the progression of AOM-induced ALF. METHODS: C57BL/6 mice were injected with AOM to produce ALF and hepatic encephalopathy. Tissue was collected at defined stages of neurological decline up to coma. Liver injury, CYP2E1 expression, oxidative stress, inflammation, apoptosis, necroptosis, and hepatocellular senescence were assessed. RESULTS: Increased hepatic necrosis and exacerbated liver injury were observed after AOM injection as mice progressed towards coma. CYP2E1 expression decreased in AOM-treated mice as liver injury progressed. Malondialdehyde, myeloperoxidase and other measures of oxidative stress were significantly increased during AOM-induced ALF. Hepatic CCL2 and tumor necrosis factor α expression increased as AOM-induced liver injury progressed. Mixed lineage kinase domain-like protein phosphorylation was increased early during the progression of AOM-induced liver injury. Measures of apoptosis and cellular senescence all increased as the time course of AOM progressed. CONCLUSION: These data support that necrosis, oxidative stress, inflammation, apoptosis, and senescence were elevated in AOM-treated mice, with inflammation being the earliest significant change.

  PublisherDOI

• Ataxia‐telangiectasia mutated activation mediates transforming growth factor beta signaling in acetaminophen‐induced liver injury in mice

  Physiological Reports · 2025-12-01

  articleOpen accessSenior author

  Acetaminophen (APAP) overdose is associated with increased transforming growth factor beta 1 (TGFβ1) signaling and elevated oxidative stress, which exacerbate DNA damage. TGFβ1 has been shown to regulate ataxia-telangiectasia mutated (ATM) signaling and DNA repair in other cell types. This study investigates the DNA damage response (DDR) during APAP-induced liver injury, focusing on ATM-mediated regulation of TGFβ1 signaling. APAP administration in vitro and in vivo resulted in DNA damage, increased ATM signaling, accumulation of γH2AX, and activation of phosphorylated ataxia telangiectasia mutated (pATM) and phosphorylated checkpoint kinase 2 (pChk2). Pretreatment with an ATM inhibitor, KU55933, attenuated APAP-induced hepatocyte damage and resulted in attenuated mothers against decapentaplegic homolog 2/3 (SMAD2/3) signaling with no changes in activated TGFβ1 levels, suggesting that ATM activation modulates TGFβ1 signaling via post-translational mechanisms. APAP was found to promote transforming growth factor beta receptor 2 (TGFβRII) stabilization through activation of phosphorylated casitas B-lineage lymphoma (p-c-cbl) and subsequent neddylation of TGFβRII, which was attenuated by inhibitors of ATM signaling or neddylation machinery. In conclusion, APAP-induced hepatic DNA damage activates an ATM-mediated response that enhances TGFβ1 signaling through stabilization of TGFβRII, and inhibition of ATM consequently reduces APAP-induced hepatic injury.

  PublisherDOI
• RETRACTED

  Retraction: Blocking H1/H2 histamine receptors inhibits damage/fibrosis in Mdr2−/− mice and human cholangiocarcinoma tumorigenesis

  Hepatology · 2025-07-02 · 1 citations

  article
  PublisherDOI

• The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy

  Journal of Immunology Research · 2025-01-01 · 5 citations

  articleOpen accessSenior authorCorresponding

  Liver disease impacts millions of Americans every year, which is compounded by the comorbidities and consequences that patients are susceptible to developing. Hepatic encephalopathy (HE) is a severe consequence of liver failure resulting in a range of cognitive deficits that heavily impact quality of life. Approximately 40% of acute liver failure (ALF) patients and 50% of chronic liver disease patients will be diagnosed with HE, and the associated prognosis is 44% and 42%, respectively. Though understanding of some of the neurologic impacts of liver impairment exists, the pathology of HE is not yet fully elucidated. Many in the field have come to appreciate the role of neuroinflammation in its pathogenesis. In this review, we have summarized recent studies investigating aspects of neuroinflammation such as microgliosis, astrogliosis, proinflammatory cytokine and chemokine production, and the involvement of the choroid plexus and meninges in HE.

  PublisherOA PDFDOI
• RETRACTED

  Retraction: GABA induces the differentiation of small into large cholangiocytes by activation of Ca2+/CaMK I-dependent adenylyl cyclase 8

  Hepatology · 2025-06-19

  article
  PublisherDOI

• Exposure to Gulf war illness-related chemicals exacerbates alcohol-induced liver damage in rodents

  Scientific Reports · 2024-07-01 · 3 citations

  articleOpen accessSenior author

  Gulf War Illness (GWI) describes a series of symptoms suffered by veterans of the Gulf war, consisting of cognitive, neurological and gastrointestinal dysfunctions. Two chemicals associated with GWI are the insecticide permethrin (PER) and the nerve gas prophylactic pyridostigmine-bromide (PB). In this study we assessed the effects of PER and PB exposure on the pathology and subsequent alcohol (EtOH)-induced liver injury, and the influence of a macrophage depletor, PLX3397, on EtOH-induced liver damage in PER/PB-treated mice. Male C57BL/6 mice were injected daily with vehicle or PER/PB for 10 days, followed by 4 months recovery, then treatment with PLX3397 and a chronic-plus-single-binge EtOH challenge for 10 days. PER/PB exposure resulted in the protracted increase in liver transaminases in the serum and induced chronic low-level microvesicular steatosis and inflammation in GWI vs Naïve mice up to 4 months after cessation of exposure. Furthermore, prior exposure to PER/PB also resulted in exacerbated response to EtOH-induced liver injury, with enhanced steatosis, ductular reaction and fibrosis. The enhanced EtOH-induced liver damage in GWI-mice was attenuated by strategies designed to deplete macrophages in the liver. Taken together, these data suggest that exposure to GWI-related chemicals may alter the liver's response to subsequent ethanol exposure.

  PublisherDOI

Recent grants

• NIH Grant R03DK088012

  NIH · $134k · 2012

• NIH Grant I01BX002638

  NIH · 2018

• NIH Grant K01DK078532

  NIH · $697k · 2013

• Dysregulation of hypothalamic neuropeptides is associated with biliary hyperplasia

  NIH · $2.7M · 2010–2022

• Molecular mechanisms of drug-induced liver injury

  NIH · $1.4M · 2018–2024

Frequent coauthors

• Gianfranco Alpini

  Richard L. Roudebush VA Medical Center

  345 shared

• Matthew McMillin

  Illinois College

  241 shared

• Gabriel Frampton

  The University of Texas at Austin

  223 shared

• Heather Francis

  Indiana University – Purdue University Indianapolis

  216 shared

• Shannon Glaser

  Texas A&M University

  205 shared

• Fanyin Meng

  China National Petroleum Corporation (China)

  187 shared

• Julie Venter

  The University of Texas at Austin

  184 shared

• Paolo Onori

  Sapienza University of Rome

  143 shared

Awards & honors

• FAASLD