About

Matthew R. Redinbo, PhD, is the Kenan Distinguished Professor of Chemistry, Biochemistry, Microbiology, and Genomics at the University of North Carolina at Chapel Hill. He grew up in New York and California and earned a BS in Biochemistry from UC Davis in 1990, with a minor in English Literature. He received his PhD in Biochemistry and structural biology from UCLA in 1995. Following his doctoral studies, he completed a postdoctoral fellowship at the University of Washington in Seattle in 1999, where he published the crystal structures of human topoisomerase I in complexes with DNA. In 1999, the same year he began his faculty position at UNC Chapel Hill, he was awarded the Burroughs Wellcome Fund Career Award in the Biological Sciences. He was tenured in 2004, promoted to Professor in 2007, and began a term as Chair of UNC’s Department of Chemistry in 2009. He was a visiting fellow at Magdalen College, Oxford from 2013 to 2014 and was named a Fellow of the American Association for the Advancement of Science (AAAS) in 2015. Throughout his career, he has been recognized with awards for his research, teaching, and mentoring. Outside of his professional work, Matt enjoys reading fiction, playing guitar, and engaging in swimming, biking, and running activities.

Research topics

• Biology
• Computer Science
• Medicine
• Biochemistry
• Immunology
• Chemistry
• Philosophy
• Data science
• Psychology
• Biophysics
• Bioinformatics
• Microbiology
• Genetics
• Library science
• Pharmacology

Selected publications

• Microbiota and kidney disease: the road ahead

  UNC Libraries · 2026-05-02

  articleOpen access
  PublisherDOI

• Glucuronidation metabolomic fingerprinting to map host-microbe metabolism

  Nature Communications · 2026-05-20

  articleOpen access

  Glucuronidation is an important detoxification pathway that operates in balance with gastrointestinal microbial β-glucuronidase (GUS) activity, which can regenerate bioactive metabolites from their glucuronidated forms. How this host-microbe interaction shapes the distribution and pool of glucuronidated metabolites (i.e., the glucuronidome) remains poorly understood. In this study, we employed pattern-filtering data science approaches in conjunction with untargeted LC-MS/MS metabolomics to map the glucuronidome in urine, serum, and colon/fecal samples from gnotobiotic and conventional mice, and in humans. We find that microbial colonization and GUS activity compress the colonic glucuronidome and expand urinary glucuronidome diversity, revealing a compartmental redistribution of glucuronidated metabolites. Reverse metabolomics of known glucuronidated chemicals and glucuronidation pattern filtering searches in public metabolomics datasets exposed the diversity of glucuronidated metabolites in human and mouse ecosystems. In summary, we present a glucuronidation fingerprint resource that provides broader access to and analysis of the glucuronidome. Together, this work establishes a scalable analytical framework and provides mechanistic insight into how microbial activity reshapes systemic glucuronidation, with implications for drug metabolism, diet-microbe interactions, and biomarker discovery.

  PublisherOA PDFDOI

• Weight Loss and Omega-3 Supplementation Modulate the Microbiome in Women with Increased Breast Cancer Risk

  Cancer Prevention Research · 2026-04-18

  articleOpen access

  Abstract Obesity is associated with gut dysbiosis, chronic inflammation, and insulin resistance. We assessed the proportional change in fecal microbial populations in a pilot study (n = 34) of peri/postmenopausal women with a body mass index ≥28 kg/m2 who were randomized to receive either 3.25 g/day of omega-3 fatty acids or a placebo during a weight loss intervention. Body composition was assessed using dual X-ray absorptiometry, and fecal and blood samples were collected. The median weight change was −10%. Among participants who lost ≥10% of their weight, those assigned to omega-3 fatty acids showed the greatest decrease in the Firmicutes:Bacteroidetes ratio and displayed favorable changes in systemic biomarkers. Notable increases in the proportional abundance of short-chain fatty acid (SCFA)–producing microbes including Phocaeicola vulgatus and Alistipes putredinis were observed in women receiving omega-3, which correlated with improvements in breast cancer biomarkers such as bioavailable estradiol, adiponectin:leptin ratio, and C-reactive protein levels. Women administered omega-3 fatty acids displayed increased % change in plasma SCFA propionate and decreased butyrate, suggesting that intervention differentially modulated circulating bacteria-derived SCFA metabolites. High-dose omega-3 fatty acids, when added to a behavioral weight loss intervention, promoted beneficial shifts in the gut microbiome and associated with improved breast cancer risk factor biomarkers. Prevention Relevance: Obesity is a modifiable risk factor for breast cancer, characterized by chronic inflammation and altered adipokines. This trial addresses the need to enhance weight loss by targeting underlying metabolic and inflammatory drivers. We show that omega-3 polyunsaturated fatty acids (eicosapentaenoic acid/docosahexaenoic acid) shift SCFA-producing microbiota, increase propionate, and correlate with improved breast cancer risk factor biomarkers.

  PublisherDOI

• 237 MICROBIAL B-GLUCURONIDASE ENZYMES FROM A CLINICAL ISOLATE OF BACTEROIDES OVATUS SUPPRESS INTESTINAL PROTEASE ACTIVITY AND IMPROVE GUT BARRIER FUNCTION

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• 237 MICROBIAL B-GLUCURONIDASE ENZYMES FROM A CLINICAL ISOLATE OF BACTEROIDES OVATUS SUPPRESS INTESTINAL PROTEASE ACTIVITY AND IMPROVE GUT BARRIER FUNCTION

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• Sex-dependent responses in mice to indomethacin-induced organ injury and gut microbiome-targeted alleviation

  Scientific Reports · 2025-10-15 · 1 citations

  articleOpen accessSenior authorCorresponding

  Nonsteroidal anti-inflammatory drugs (NSAIDs) are used widely but produce gastrointestinal (GI) toxicities in both short- and long-term users. Previous studies have shown that the intestinal microbiota play an important role in gut damage and that gut microbial β-glucuronidase (GUS) inhibitors can alleviate NSAID-induced injury in male mice by blocking the GI reactivation of NSAID-glucuronides. Here, in both male and female C57BL/6 mice, we examine the effects of indomethacin alone and with the GUS inhibitor UNC10201652. Oral delivery of 5 mg/kg body weight indomethacin over 5 days decreased body weight, induced colonic and hepatic inflammatory cytokine gene expression, and enlarged the spleens of both male and female mice. However, sex-specific inflammatory responses to indomethacin were observed, with males demonstrating more colonic injury while females presented greater splenic and hepatic toxic responses. Females also showed a unique indomethacin-induced bloom of fecal Verrucomicrobia as measured by 16S rRNA metagenomic sequencing. UNC10201652 alleviated aspects of these indomethacin-induced toxicities, including features of the male-specific colonic damage and the female-specific compositional changes and spleen and liver toxicities. Thus, GI and non-GI tissues in male and female mice respond distinctly to indomethacin-induced damage. These findings advance our understanding of how sex impacts systemic responses to xenobiotic exposure and may lead to improved therapeutic outcomes with these widely used drugs.

  PublisherOA PDFDOI

• Structural Insights into Selectively Targeting <i>Candida albicans</i> Hsp90

  Biochemistry · 2025-05-21 · 1 citations

  articleOpen accessSenior authorCorresponding

  The threat of drug-resistant pathogens continues to rise and underscores the need for new antimicrobial and antifungal strategies. Diverse chemical scaffolds have been shown with high affinity to bind the human heat-shock protein Hsp90. Orthologous proteins are present in microbial pathogens and have been shown to be particularly abundant in these organisms, suggesting they may serve as therapeutic targets. Here, we examine the potency and selectivity of human Hsp90 ligands for their capacity to bind to the nucleotide binding domain of Hsp90 from the pathogenic fungi, Candida albicans. Using a series of biochemical, structural, and fragment and in silico screening investigations, we define key chemical features that lead to effective C. albicans Hsp90 (CaHsp90) binding. We support these studies with crystal structures of five diverse human Hsp90 ligands in complex with CaHsp90, as well as the structure of this protein with a nonhydrolyzable ATP analog. We demonstrate the structural basis for the selectivity of the human Hsp90 inhibitor TAS116 for CaHsp90, features that may be exploited in the future development of improved CaHsp90 inhibitors.

  PublisherOA PDFDOI

• Emerging gut microbial glycoside hydrolase inhibitors

  RSC Chemical Biology · 2025-01-01 · 6 citations

  reviewOpen accessSenior author

  The human gut microbiota has been linked to numerous diseases through their metabolism of molecules in the gastrointestinal tract. Post-translational glycosylation is applied to many secreted proteins, including mucins and immunoglobulins, and glycosides are present in diet and generated by host metabolism systems. Thus, glycosides are key targets for degradation by gut microbial glycoside hydrolases (GHs). Indeed, diverse xenobiotic compounds, including therapeutics and dietary phytochemicals, along with endobiotics like neurotransmitters and hormones, are conjugated to monosaccharides making them substrates for GH enzymes. A range of GH inhibitors have been developed to study lysosomal storage diseases, treat viral infections, and to address type II diabetes. Recently, GH inhibitors have offered promising avenues for investigating gut microbial GHs and their influence on host health and disease. In this review we describe the growing classes of GH inhibitors and their applications in studying gut microbial GHs that target host-derived glycans and dietary and drug-xenobiotic molecules. We also review the use of GH-targeting activity-based probes to pinpoint specific proteins expressed by the gut microbiota that influence molecular and phenotypic outcomes. As we deepen our understanding of gut microbial GH function, we will further elucidate the roles played by the microbiota in host physiology and disease toward potential therapeutic interventions that target non-host factors in acute and chronic disorders.

  PublisherOA PDFDOI

• Sex-Dependent Responses in Mice to Indomethacin-Induced Injury and Gut Microbiome-Targeted Alleviation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-27

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Nonsteroidal anti-inflammatory drugs (NSAIDs) are used widely but produce gastrointestinal (GI) toxicities in both short- and long-term users. Previous studies have shown that the intestinal microbiota play an important role in gut damage and that gut microbial β-glucuronidase (GUS) inhibitors can alleviate NSAID-induced injury in male mice by blocking the GI reactivation of NSAID-glucuronides. Here, in both male and female C57BL/6 mice, we examine the effects of indomethacin alone and with the GUS inhibitor UNC10201652. Oral delivery of 5 mg/kg body weight indomethacin over five days decreased body weight, induced colonic and hepatic inflammatory cytokine gene expression, and enlarged the spleens of both male and female mice. However, sex-specific inflammatory responses to indomethacin were observed, with males demonstrating more colonic injury while females presented greater splenic and hepatic toxic responses. Females also showed a unique indomethacin-induced bloom of fecal Verrucomicrobia as measured by 16S rRNA metagenomic sequencing. UNC10201652 alleviated aspects of these indomethacin-induced toxicities, including features of the male-specific colonic damage and the female-specific compositional changes and spleen and liver toxicities. Thus, GI and non-GI tissues in male and female mice respond distinctly to indomethacin-induced damage. These findings advance our understanding of how sex impacts systemic responses to xenobiotic exposure and may lead to improved therapeutic outcomes with these widely used drugs.

  PublisherOA PDFDOI

• Glucuronidation Metabolomic Fingerprinting to Map Host-Microbe Metabolism

  Research Square · 2025-04-08 · 2 citations

  preprintOpen accessSenior author
  PublisherOA PDFDOI

Recent grants

• NIH Grant R01DK062229

  NIH · $1.7M · 2008

• Structural Basis for Hormone and Neurotransmitter Processing by Gut Microbial Enzymes

  NIH · $1.5M · 2019–2024

• NIH Grant R01CA098468

  NIH · $3.9M · 2020

• NIH Grant R01AI078924

  NIH · $1.9M · 2014

• NIH Grant R01CA207416

  NIH · $1.7M · 2022

Frequent coauthors

• William G. Walton

  University of North Carolina at Chapel Hill

  57 shared

• Sridhar Mani

  Albert Einstein College of Medicine

  38 shared

• Philip M. Potter

  33 shared

• Steven A. Kliewer

  The University of Texas Southwestern Medical Center

  30 shared

• Wim G. J. Hol

  University of Washington

  30 shared

• Parth B. Jariwala

  30 shared

• Linda B. Moore

  GlaxoSmithKline (United States)

  28 shared

• James J. Champoux

  University of Washington

  26 shared

Labs

• Redinbo LabPI

Education

• PhD, Biochemistry, Chemistry and Biochemistry

  University of California Los Angeles

  1995

• BS, Biochemistry

  University of California Davis

  1990

Awards & honors

• UNC Tanner Award for Excellence in Undergraduate teaching (2…
• UNC Research Outstanding Mentor Award (2018)
• Fellow, AAAS (2013)
• Academic Leadership Fellow, UNC (2011)
• Academic Leadership Fellow (2010)