About

Susan Kay Murphy is an Associate Professor in Obstetrics and Gynecology at Duke University. She serves as the Chief of the Division of Reproductive Sciences within the Department of Obstetrics and Gynecology. Additionally, she holds positions as an Associate Professor in Pathology and in the Division of Environmental Natural Sciences, and is a member of the Duke Cancer Institute. Her professional roles indicate a focus on reproductive sciences, with involvement in research and clinical activities related to obstetrics and gynecology.

Research topics

• Medicine
• Biology
• Genetics
• Internal medicine
• Physiology
• Psychiatry
• Andrology
• Psychotherapist
• Demography
• Oncology
• Clinical psychology
• Endocrinology
• Psychology

Selected publications

• UV irradiation alters TFAM binding specificity and compaction of DNA

  eLife · 2026-03-25

  articleOpen access

  Mitochondria lack nucleotide excision repair; however, mitochondrial DNA (mtDNA) is resistant to mutation accumulation following DNA damage. These observations suggest additional damage sensing or protection mechanisms. Transcription Factor A, Mitochondrial (TFAM) compacts mtDNA into nucleoids and binds differentially to certain forms of DNA damage. As such, TFAM has emerged as a candidate for protecting mtDNA or sensing damage. To examine the possibilities that TFAM might protect DNA from damage or act as a damage sensing protein for irreparable forms of mtDNA damage, we used live-cell imaging and HeLa cell-based assays, atomic force microscopy (AFM), and high-throughput protein-DNA binding assays to characterize the binding properties of human TFAM to ultraviolet-C (UVC) irradiated DNA and the cellular consequences of UVC irradiation. Our cell data show increased TFAM mRNA after exposure and suggest an increase in mtDNA degradation without a loss in mitochondrial membrane potential that might trigger mitophagy. Our protein-DNA binding assays indicate a reduction in sequence specificity of TFAM following UVC irradiation and a redistribution of TFAM binding throughout the mitochondrial genome. Our AFM data show increased compaction of DNA by TFAM in the presence of damage. Despite the TFAM-mediated compaction of mtDNA in vitro, we do not observe any protective effect of increased TFAM protein on DNA damage formation in cells or in vitro. Increased TFAM protein did not alter levels of mtDNA damage over time after UVC exposure in vivo, but knockdown of TFAM did alter mtDNA damage levels in HeLa cells both at baseline and after UVC exposure. Taken together, these studies indicate that UVC-induced DNA damage alters TFAM binding and promotes compaction by TFAM in vitro. We hypothesize that TFAM may act as a damage sensing protein in vivo, sequestering damaged genomes to prevent mutagenesis by facilitating removal or suppression of replication.

  PublisherDOI

• Author response: UV irradiation alters TFAM binding specificity and compaction of DNA

  2026-03-25

  peer-reviewOpen access
  PublisherDOI

• Prenatal Cannabis and Tobacco: Studies in Animal Models

  Advances in experimental medicine and biology · 2026-01-01

  book-chapter
  PublisherDOI

• Sa2066 URINARY CANNABINOID METABOLITE LEVELS IN CHRONIC LIVER DISEASE: A CROSS-SECTIONAL ANALYSIS OF THE SOUTHERN LIVER HEALTHY STUDY (STRIVE)

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• Environmental exposures and epigenetic alterations in common chronic diseases: insights and challenges

  Current Zoology · 2026-01-01

  articleOpen accessSenior author

  Exposure to environmental factors including contaminants and social conditions is implicated in a substantial proportion of common non-communicable diseases, and data from model systems repeatedly demonstrate that the process from environmental contributions to common chronic disease risk is mediated through maladaptive epigenetic responses. The field of environmental epigenetics leverages multiple disciplines to advance our understanding of environmental impacts on epigenomic processes to enhance etiologic investigation, guide biomarker discovery, and identify mechanisms of action that ultimately lead to behavioral and or therapeutic interventions. This article discusses examples of emerging research on the links between three common life course exposures linked to common non-communicable diseases, and their associated epigenetic modifications, with a major focus on DNA methylation-the most studied in humans. It also outlines current challenges when interpreting the accumulating body of knowledge, including the lack of consensus on regions reported to be targeted by these environmental exposures. Finally, given that the strongest predictors of epigenetic states are age and cell/tissue type, strategies to build novel platforms using existing technologies to surmount some of these challenges are discussed. Together, these advances in environmental epigenetics are paving the way for groundbreaking developments toward improved precision in developing prevention and intervention strategies to reduce common non-communicable disease morbidity and mortality.

  PublisherOA PDFDOI

• Sa2066 URINARY CANNABINOID METABOLITE LEVELS IN CHRONIC LIVER DISEASE: A CROSS-SECTIONAL ANALYSIS OF THE SOUTHERN LIVER HEALTHY STUDY (STRIVE)

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• Ascites protects against ferroptosis and enables the peritoneal growth of ovarian cancer

  Nature Communications · 2026-05-11

  articleOpen access

  The peritoneum is a frequent site of metastasis in ovarian cancer (OVCA), often accompanied by the accumulation of ascites in the peritoneal cavity. Despite its prevalence, ascites and its role in the peritoneal growth of OVCA remain poorly understood. OVCA cells are vulnerable to ferroptosis, a type of cell death caused by lipid hydroperoxides, raising the question of how these ferroptosis-sensitive cells survive during metastasis. Here, we show that ascites from female donors protects OVCA cell lines, patient-derived tumor cells, and organoids against ferroptosis and enhances peritoneal tumor growth in female mice. Mechanistically, ascites downregulates 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), contributing to increased lipid droplets. Additionally, upon ferroptosis induction, ascites represses upregulation of the transferrin receptor TFRC, thereby decreasing labile iron levels. Furthermore, lipid-lowering fibrates reverse ascites-induced changes and attenuate peritoneal growth in female mice. These findings identify ascites-mediated ferroptosis protection as a key mechanism in OVCA metastasis and a potential therapeutic vulnerability.

  PublisherOA PDFDOI

• UV irradiation alters TFAM binding specificity and compaction of DNA

  UNC Libraries · 2026-04-02

  articleOpen access

  Mitochondria lack nucleotide excision repair; however, mitochondrial DNA (mtDNA) is resistant to mutation accumulation following DNA damage. These observations suggest additional damage sensing or protection mechanisms. Transcription Factor A, Mitochondrial (TFAM) compacts mtDNA into nucleoids and binds differentially to certain forms of DNA damage. As such, TFAM has emerged as a candidate for protecting mtDNA or sensing damage. To examine the possibilities that TFAM might protect DNA from damage or act as a damage sensing protein for irreparable forms of mtDNA damage, we used live-cell imaging and HeLa cell-based assays, atomic force microscopy (AFM), and high-throughput protein-DNA binding assays to characterize the binding properties of human TFAM to ultraviolet-C (UVC) irradiated DNA and the cellular consequences of UVC irradiation. Our cell data show increased TFAM mRNA after exposure and suggest an increase in mtDNA degradation without a loss in mitochondrial membrane potential that might trigger mitophagy. Our protein-DNA binding assays indicate a reduction in sequence specificity of TFAM following UVC irradiation and a redistribution of TFAM binding throughout the mitochondrial genome. Our AFM data show increased compaction of DNA by TFAM in the presence of damage. Despite the TFAM-mediated compaction of mtDNA in vitro, we do not observe any protective effect of increased TFAM protein on DNA damage formation in cells or in vitro. Increased TFAM protein did not alter levels of mtDNA damage over time after UVC exposure in vivo, but knockdown of TFAM did alter mtDNA damage levels in HeLa cells both at baseline and after UVC exposure. Taken together, these studies indicate that UVC-induced DNA damage alters TFAM binding and promotes compaction by TFAM in vitro. We hypothesize that TFAM may act as a damage sensing protein in vivo, sequestering damaged genomes to prevent mutagenesis by facilitating removal or suppression of replication.

  PublisherDOI

• Abstract 4803: Ascites protects against ferroptosis and enables the peritoneal spread of ovarian cancer

  Cancer Research · 2026-04-03

  article

  Abstract One of the most common sites of metastasis in ovarian cancer (OVCA) is the peritoneum. Often, this spread is accompanied by the accumulation of a fluid called ascites in the peritoneal cavity. Despite its common occurrence in metastatic OVCA patients, ascites and its influence on the peritoneal spread of OVCA are poorly understood. Interestingly, OVCA cells are vulnerable to ferroptosis, a type of cell death caused by lipid hydroperoxides. Hence, how these ferroptosis-sensitive OVCA cells persist in their spread to the peritoneum remains unknown. Here, we show that ascites robustly protects OVCA cell lines, patient-derived tumor cells and organoids against ferroptosis and enhances the peritoneal spread of OVCA cells in mice. Mechanistically, ascites downregulates the mitochondrial enzyme, 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), which contributes to an increase in lipid droplets. Additionally, upon ferroptosis induction, ascites represses the upregulation of the transferrin receptor, TFRC, thereby decreasing cellular labile iron levels. Furthermore, we show that lipid-lowering fibrates reverse cellular changes induced by ascites, and they attenuate the peritoneal spread of OVCA cells in mice. Our findings implicate the importance of ascites in ferroptosis protection and the peritoneal spread of OVCA, and they suggest that targeting the ferroptosis protection by ascites may present a novel therapeutic approach to limit OVCA metastasis. Citation Format: Yasaman Setayeshpour, Ssu-Yu Chen, Divya L. Dayanidhi, Yunji Lee, Shao-Chin Wu, Juan J. Aristizabal-Henao, Jianli Wu, Chao Chieh (Jerry) Lin, Nazanin Setayeshpour, Chiara Federico, Alexander A. Mestre, Michael A. Kiebish, Andrew Berchuck, David S. Hsu, Zhiqing Huang, Susan K. Murphy, Jen-Tsan Ashley Chi. Ascites protects against ferroptosis and enables the peritoneal spread of ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4803.

  PublisherDOI

• UV irradiation alters TFAM binding to mitochondrial DNA

  eLife · 2025-11-19

  articleOpen access

  Mitochondria lack nucleotide excision repair; however, mitochondrial DNA (mtDNA) is resistant to mutation accumulation following DNA damage. These observations suggest additional damage sensing or protection mechanisms. Transcription Factor A, Mitochondrial (TFAM) compacts mtDNA into nucleoids and binds differentially to certain forms of DNA damage. As such, TFAM has emerged as a candidate for protecting mtDNA or sensing damage. To examine the possibilities that TFAM might protect DNA from damage or act as a damage sensing protein for irreparable forms of mtDNA damage, we used live-cell imaging, cell-based assays, atomic force microscopy (AFM), and high-throughput protein-DNA binding assays to characterize the binding properties of TFAM to ultraviolet-C (UVC) irradiated DNA and the cellular consequences of UVC irradiation. Our cell data show increased TFAM mRNA after exposure and suggest an increase in mtDNA degradation and turnover without a loss in mitochondrial membrane potential that might trigger mitophagy. Our protein-DNA binding assays indicate a reduction in sequence specificity of TFAM following UVC irradiation and a redistribution of TFAM binding throughout the mitochondrial genome. Our AFM data show increased compaction of DNA by TFAM in the presence of damage. Despite the TFAM-mediated compaction of mtDNA, we do not observe any protective effect of increased compaction on DNA damage formation in cells or in vitro. Taken together, these studies indicate that UVC-induced DNA damage alters TFAM binding and promotes compaction by TFAM, suggesting that TFAM may act as a damage sensing protein, sequestering damaged genomes to prevent mutagenesis by facilitating removal or suppression of replication.

  PublisherDOI

Recent grants

• Duke University Program in Environmental Health

  NIH · $3.8M · 2013–2029

• NIH Grant P01ES022831

  NIH · $7.9M · 2019

• NIH Grant R01CA14298302S1

  NIH · $86k · 2013

• NIH Grant F32CA094668

  NIH · $82k · 2003

• Follow-up and Maintenance of the Newborn Epigenetics STudy (NEST) Cohort

  NIH · $1.9M · 2018–2024

Frequent coauthors

• Cathrine Hoyo

  North Carolina State University

  282 shared

• Zhiqing Huang

  223 shared

• Tsukasa Baba

  Iwate Medical University

  162 shared

• Noriomi Matsumura

  131 shared

• Lu Gao

  128 shared

• Rachel L. Maguire

  North Carolina State University

  117 shared

• Ikuo Konishi

  Kyoto Medical Center

  114 shared

• Andrew Berchuck

  97 shared

Education

• PhD, Microbiology and Immunology

  Wake Forest University

  1998