About

Dr. Hugh Taylor is the Anita O'Keeffe Young Professor and Chair of the Department of Obstetrics, Gynecology, and Reproductive Sciences at Yale School of Medicine, as well as the Chief of Obstetrics and Gynecology at Yale-New Haven Hospital. He is also a Professor of Molecular, Cellular, and Developmental Biology at Yale University. His clinical interests include IVF, infertility, endometriosis, implantation, menopause, uterine anomalies, and Asherman's syndrome. Dr. Taylor's research centers on endometriosis and fibroids, with a focus on uterine development, endocrine disruption, stem cells, and the molecular mechanisms underlying reproductive health conditions. His laboratory has identified novel mechanisms involved in endometriosis, including the roles of stem cells, epigenetics, and microRNA, and has developed therapies for the disease. He has demonstrated the contribution of exogenous stem cells from bone marrow and other tissues to endometrial regeneration and explored their potential in regenerative medicine. Additionally, his work on uterine development has elucidated the molecular mechanisms by which the Mullerian duct differentiates into various components of the female reproductive tract, highlighting the role of HOX genes and the impact of environmental estrogens like BPA and DES on reproductive development through epigenetic reprogramming. Dr. Taylor has published over 400 articles, received ten NIH research grants, and served as president of the Society for Reproductive Investigation and the American Society for Reproductive Medicine in 2021. He is a member of the National Academy of Medicine.

Research topics

• Medicine
• Biology
• Internal medicine
• Endocrinology
• Genetics
• Sociology
• Bioinformatics
• Political Science
• Obstetrics
• Virology
• Economics
• Economic growth
• Demography
• Development economics
• Geography
• Telecommunications
• Chemistry
• Surgery
• Cancer research
• Cell biology
• Physiology
• Gynecology
• Environmental health
• Pathology

Selected publications

• Autologous cell therapy with CD133+ bone marrow-derived stem cells for Asherman Syndrome: a phase 1/2 trial

  Nature Communications · 2026-01-02

  articleOpen access

  Autologous CD133+ bone marrow-derived stem cell (BMDSC) therapy has been designated as an Orphan Drug by the EMA and FDA for the treatment of Asherman Syndrome (AS). This phase 1/2, non-randomized, open-label, single-arm trial assessed the safety and efficacy of this novel therapy in 20 infertile women with moderate to severe AS, unresponsive to prior hysteroscopic treatments. Primary endpoints were safety and tolerability over 15 months follow-up, including during pregnancy and after live birth. The therapy was well tolerated with a mean dosage of 125.41 × 106 cells, with no treatment-related serious adverse events and only reversible events such as arm pain, headache, and nausea. In pregnant patients, minor obstetric complications were reflux-related cough (n = 1), gestational diabetes (n = 2), cervical shortening requiring pessary placement (n = 2), and postpartum placenta accreta (n = 1). No preterm labor occurred, and all six newborns remained free of significant adverse events. Our findings suggest that autologous CD133 + BMDSC therapy is a safe and effective treatment for AS. Clinical trial registration (Eudra CT): 2016-003975-23 The authors present the results of a phase I/II clinical trial using autologous CD133+ bone marrow stem cell therapy to restore fertility in patients with Asherman Syndrome. The intervention was safe and showed promising results for the restoration of menstruation and reproductive function.

  PublisherDOI

• Redefining the contribution of retrograde menstruation to endometriosis: single-cell analysis of endometriotic lesions suggests a process more complex than simple autografting

  Molecular Medicine · 2026-02-19

  articleOpen accessSenior author

  Endometriosis is a common gynecological disorder causing pelvic pain and infertility. While generally attributed to peritoneal implants of endometrium derived from retrograde menstruation, the contribution of cells from the circulation to the development of endometriotic lesions is unknown. Here, we describe the infiltration of circulating cells into endometriotic lesions. Experimental endometriosis was induced in mice by transplanting uterine tissue from donor mice that express green fluorescence protein (GFP) into peritoneal cavity of recipient wild type mice. Lesions were collected after 18-weeks, and single cell suspensions were subjected to for single-cell sequence analysis. 10,000 cells were tagged per lesion and sequenced. Data was analyzed for GFP sequence using Seurat package in R studio. Tagged endometriosis cells showed that 35% expressed GFP while 65% did not, surprisingly indicating that most cells are derived from the circulation rather than the transplanted endometrium. Cell cluster analysis showed that the host-derived infiltrated cells consisted of Natural Killer (NK) cells, B cells, macrophages (M1 and alveolar), T cells, fibroblasts, neutrophils and endothelial cells. The endometriotic lesions contained twofold more endogenously derived host cells than cells originating from the uterine allografts. The top 10 genes in each host cell cluster that entered the lesions endogenously were analyzed for their predicted functions in the development of endometriosis. This study demonstrates that most of the cells in endometriotic lesions are derived from the host from the host circulation, rather than carried with the lesion. The majority are immune cells suggesting novel alternative ways to treat the disease.

  PublisherDOI

• Author’s Reply

  Journal of Minimally Invasive Gynecology · 2026-01-01

  articleSenior author
  PublisherDOI

• Sex-specific differences in liver DNA methylation patterns and epigenetic aging in mice

  American Journal of Physiology-Gastrointestinal and Liver Physiology · 2026-02-16 · 1 citations

  articleSenior authorCorresponding

  Males and females are known to age differently and develop certain diseases at different rates. Here, we examined the livers of aged male and female mice to see if they show different DNA methylation patterns. We found that aged male and female mice had distinct DNA methylation patterns at specific genes. Interestingly, most of these methylation differences were not present in younger mice, suggesting that sex differences in the genome may change with age.

  PublisherDOI

• SUN-155 The Prevalence of Pathogenic Variants in Medically Actionable Genes Among Women with Idiopathic Hypogonadotropic Hypogonadism/Kallmann Syndrome

  Journal of the Endocrine Society · 2025-10-01

  articleOpen access

  Abstract Disclosure: J.M. Kwal: None. L.P. Chorich: None. Z. Hawkins: None. L. Grater: None. J. Knight: None. H.S. Taylor: None. L.C. Layman: None. Background: Idiopathic Hypogonadotropic Hypogonadism (IHH) is an endocrine disorder characterized by impaired GnRH neuron migration along olfactory axons (Kallmann syndrome—KS) or defects in the production or action of gonadotropin-releasing hormone (GnRH). This results in low or inappropriately normal serum concentrations of luteinizing hormone and follicle-stimulating hormone and deficient gonadal ѕtеrоiԁs and subsequent infertility. Our group previously showed that other types of infertility are associated with an increased prevalence of pathogenic and likely pathogenic (P/LP) variants in medically actionable genes (MAGs) vs. controls when exome sequencing was performed. Objective: We hypothesize that a diagnosis of IHH/KS could also increase the risk of P/LP variants in these MAGs, which predispose to future medical illness. Methods: Exome sequencing was performed on 144 patients with IHH/KS. We previously sequenced these 144 patients, and 19% of them had P/LP variants in known IHH/KS genes, which was the primary indication for sequencing. In this study we wanted to determine if they had P/LP variants in MAG. Variants were filtered to include only those in the 81 genes from the ACMG SF v3.2 list for secondary findings (i.e., MAGs). Sanger sequencing is being performed to confirm results. The prevalence of these variants was compared to public control data from the UK Biobank and eMERGE databases. Power analysis at an alpha of 0.05 to detect a 4% (or 3-fold) difference in the prevalence of P/LP variants between the IHH/KS cohort and the national databases would require 141 patients at 80% power. Results: We showed that 5/144 (3.5%) individuals with IHH/KS had at least one P/LP variant in 4 MAGs. Of these, 2/144 (1.4%) persons had P/LP variants in cancer-related genes (TSC1); 4/144 (2.8%) had variants in cardiovascular disease genes (SCN5A, MYBPC3), and 1/144 (0.7%) had P/LP variants in inborn errors of metabolism (RYR1). One person, not included, had over 13 variants, which was thought to be artifact. There were two additional people who were heterozygous for HFE. This was not sufficient to cause medical illness since hemochromatosis is autosomal recessive. The prevalence of our variants in MAGs was 1.4-fold higher than in the UK Biobank and 1.8-fold higher than in the eMERGE database when 59 MAGs are included. However, this was not statistically different than the 2.5% and 2% from the UKB and eMERGE control databases. Conclusions: Individuals with IHH/KS had a 3.5% detection rate of P/LP variants in MAG, which did not differ from the prevalence in the general population. These findings suggest that secondary findings in IHH/KS are not a risk factor for genetic causes affecting future medical illness. Presentation: Sunday, July 13, 2025

  PublisherOA PDFDOI

• MicroRNAs associated with adenomyosis promote endometrial epithelial cell migration via MMP-2 and MMP-9 upregulation

  Biology of Reproduction · 2025-11-10

  articleOpen access

  Adenomyosis is a common gynecological disorder characterized by the presence of endometrial tissue in the myometrium, causing chronic pelvic pain and abnormal bleeding. Although dysregulated microRNAs (miRNAs) in stromal cells of adenomyosis patients have been implicated in disease-associated extracellular matrix (ECM) remodeling, their role in regulating endometrial epithelial cell (EEC) behavior remains poorly understood. This study investigated the effect of selected adenomyosis- and endometriosis-associated miRNAs on EEC migration and matrix metalloproteinase (MMP) expression. Ishikawa cells, a human endometrial epithelium-like cell line, were transfected with mimics and inhibitors of Let-7b, miR-451a, miR-125b, miR-7 and miR-150. Cell migration was assessed using wound healing assays. MMP-2 and MMP-9 mRNA expression were quantified by quantitative real-time polymerase chain reaction, while protein production and secretion were evaluated by enzyme-linked immunosorbent assay. Transfection with Let-7b-5p inhibitor and miR-451a, miR-125b-1 and miR-150 mimics significantly enhanced cell migration and led to increased MMP-2 and MMP-9 mRNA expression, intracellular protein levels and secretion. These findings suggest that these miRNAs promote EEC migration and ECM remodeling through MMP upregulation, pointing to a potential mechanism for lesion formation in adenomyosis. Future research should seek to validate these findings in primary EECs and explore the therapeutic potential of targeting miRNA-MMP pathways for adenomyosis treatment.

  PublisherOA PDFDOI

• CD34+KLF4+ Stromal Stem Cells Contribute to Endometrial Regeneration and Repair

  Cell Reports · 2025-06-17

  erratumOpen access
  PublisherOA PDFDOI

• slideimp: Efficient Imputation for DNA Methylation Data

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-17

  articleOpen access

  Abstract Motivation There is a growing need for efficient imputation methods for high-dimensional DNA methylation (DNAm) datasets. Existing microarray imputation approaches, such as k-nearest neighbors (K-NN) or principal component analysis (PCA)-based methods, provide high accuracy but can be computationally intensive, while methods for whole-genome data are not designed for large cohorts. We developed slideimp, an R package that implements sliding window, groupable, parallelized K-NN and optimized PCA imputation to address these limitations. Results Benchmarks on microarray DNAm datasets demonstrate that slideimp achieves up to 150x faster runtime and 10x-100x lower memory usage while maintaining comparable or superior accuracy over existing methods and implementations. For K-NN and PCA imputation, slideimp supports grouped imputation which enhances imputation efficiency and accuracy. In a whole-genome dataset, sliding window K-NN imputation substantially increased the correlation of the Horvath 2013 clock with chronological age from 0.131 to 0.477. Additional features include targeted imputation of CpG subsets for K-NN and estimation of imputation accuracy via repeated cross-validation. The efficient and flexible DNAm imputation methods implemented by slideimp can easily be applied to other high-dimensional data types. Availability and Implementation The code to fully reproduce all analyses presented in this paper is available on GitHub at https://github.com/hhp94/slideimp_paper . The R package slideimp is also available on GitHub at https://github.com/hhp94/slideimp . Supplemental figures are available online.

  PublisherDOI

• Endometrial Injury and Its Rescue by Mesenchymal Stem Cells Is Dependent on Estrous Cycle Phase

  Journal of Cellular and Molecular Medicine · 2025-11-01 · 1 citations

  articleOpen accessSenior author

  ABSTRACT Asherman Syndrome (AS) is caused by injury to the endometrium leading to uterine scarring, decreased menstruation and infertility; it typically occurs after surgical curettage of the uterus. AS is treated surgically albeit with limited success. Administration of bone marrow‐derived mesenchymal stem cells (MSCs) has recently been demonstrated to restore uterine function in AS; however, there is no data available on the role of the estrous cycle phase on outcomes. Here, we describe endometrial injury during estrus or diestrus, its differential effect on fertility, and its response after bone marrow MSC treatment to reverse the infertility in a murine model. Endometrial injury in the estrus phase did not affect fertility outcomes whereas injury in the diestrus phase resulted in infertility. Bone marrow (BM)‐derived MSC treatment without injury in the estrus or diestrus phase did not affect the pregnancy outcomes. BM MSC treatment following endometrial injury in the diestrus phase restored fertility. Immunofluorescence analysis revealed that vimentin or cytokeratin‐positive BM‐derived cells in the uterus were extremely rare. BM MSC treatment after injury increased CD45 + cells, indicating a role for immunomodulation in endometrial repair. Finally, qRT‐PCR showed that Ccl3 , Il‐1β and Mmp3 gene expression was significantly higher in the endometrium of the injury + BM MSC group than in other groups. In summary, injury to the endometrium during the diestrus phase results in infertility that can be restored by the treatment of BM MSCs. The therapeutic effect of BM MSCs on the endometrium appears to be mediated primarily by immunomodulation rather than BM MSC engraftment.

  PublisherOA PDFDOI

• THE PREVALENCE OF PATHOGENIC VARIANTS IN MEDICALLY ACTIONABLE GENES AMONG INDIVIDUALS WITH IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM/KALLMANN SYNDROME

  Fertility and Sterility · 2025-12-01

  article
  PublisherDOI

Recent grants

• NIH Grant R01HD036887

  NIH · $1.4M · 2011

• NIH Grant R01HD076422

  NIH · $2.0M · 2018

• NIH Grant R01ES010610

  NIH · $2.9M · 2012

• The Yale WRHR Career Development Center

  NIH · $7.4M · 2004–2030

• NIH Grant K11HD001003

  NIH · $453k · 1998

Frequent coauthors

• Ahmed M. Soliman

  516 shared

• Linda C. Giudice

  Mayo Clinic

  482 shared

• David F. Archer

  Eastern Virginia Medical School

  475 shared

• Nelson B. Watts

  Mercy Health

  468 shared

• Maurício Simões Abrão

  Universidade de São Paulo

  458 shared

• Brittany Schwefel

  AbbVie (Japan)

  453 shared

• Kristof Chwalisż

  Michigan State University

  453 shared

• Nicholas Leyland

  Activation Laboratories

  451 shared

Education

• Fellow, Reproductive Endocrinology and Infertility

  Yale University

  1998

• Post Doc Fellow, Mol Biophysics and Biochem

  Yale University

  1996

• Resident, OB GYN

  Yale University

  1992

• MD

  University of Connecticut Health Center

  1988

• BA

  Yale University

  1983

Awards & honors

• President of the Society for Reproductive Investigation
• President of the American Society for Reproductive Medicine…
• Member of the National Academy of Medicine