About

Kurt Zimmerman, DVM, PhD, DACVP, is a Professor of Pathology and Associate Head for Faculty Affairs at the Virginia-Maryland College of Veterinary Medicine, Virginia Tech. His educational background includes a Doctor of Veterinary Medicine degree from Purdue University obtained in 1984, a Veterinary Clinical Pathology Residency completed in 2001, and a PhD in Veterinary Medical Science/Medical Informatics earned in 2003 from Virginia Tech. He is board certified as a Diplomate of the American College of Veterinary Pathologists in both anatomic pathology (2008) and clinical pathology (2001). His research interests focus on medical expert systems, medical knowledge representation, knowledge discovery and machine learning algorithms, medical decision making, and diagnostic pathology. Dr. Zimmerman has held various professional roles at Virginia Tech since 2002, progressing from Assistant Professor to his current position, and has also worked as an informatics research fellow at the National Library of Medicine. His professional memberships include the American Veterinary Medical Association, the American College of Veterinary Pathology, the American Medical Informatics Association, and the American Society of Veterinary Clinical Pathology. He holds veterinary licenses in multiple states including Virginia. His work is centered in the Department of Biomedical Sciences and Pathobiology within the Virginia-Maryland College of Veterinary Medicine.

Research topics

• Internal medicine
• Medicine
• Endocrinology
• Chemistry
• Pathology
• Biochemistry
• Cardiology
• Biology

Selected publications

• The impact of 3rd party vessel allograft in kidney transplantation

  Human Immunology · 2025-09-01

  article
  PublisherDOI

• Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development

  Nature Communications · 2025-07-29 · 4 citations

  articleOpen access

  Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. Inhibition of a single miR-200 family member within the cluster results in defects of the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family results in a ventricular septal defect and embryonic lethality by embryonic day (E)16.5. Inhibition of each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing reveals an immature cardiomyocyte cell state, suggesting reduced differentiation of these cells. The miR-200 family members are critical regulators of early cardiac development through maintaining cardiomyocyte differentiation and maturation. In this report, we identify several transcription factors regulated by miR-200 during heart development, a role for miR-200 in specific heart defects, and an abnormal cardiomyocyte population. Key cardiac transcription factors require precise regulation for heart development and function. Here, the authors show that the miR-200 family controls cardiomyocyte differentiation and maturation, with its loss causing structural heart defects.

  PublisherOA PDFDOI

• Sertraline exposure during development may impact post‐myocardial infarction survival in adult mice

  Physiological Reports · 2025-11-01

  articleOpen access

  This study examines sex-specific effects of developmental sertraline exposure on cardiac function and gene expression before and after myocardial infarction (MI) in mice. Female C57BL/6 mice (10 weeks) received intraperitoneal sertraline (5 mg/kg/day, n = 37) or saline (n = 20) before mating, during pregnancy, and postnatally to pups (1.5 mg/kg/day, postnatal Days 0-14). MI in offspring was induced at 10 weeks by left coronary artery ligation. Randomly chosen offspring (sham n = 8 and MI n = 26 per sex) underwent baseline echocardiography and at 10 weeks post-MI if surviving. Serotonin- and estrogen-related gene expression was analyzed. Before MI, sertraline-exposed females had lower heart rate (649.1 ± 102.0 vs. 692.9 ± 38.4 bpm, n = 34), increased end-systolic volume, and reduced ejection fraction (80.7 ± 6.3% vs. 83.9 ± 3.5%; p < 0.05). Exposed males also had lower heart rates (665.9 ± 32.7 vs. 683.3 ± 47.9 bpm, n = 34, p < 0.05). Post-MI, both sexes remodeled similarly (scar size, ischemic-zone fraction); sertraline-exposed males had higher scar-zone collagen (p < 0.05) and a nonsignificant lower survival trend than females. Sertraline altered serotonin-related gene expression (Htr2a, Htr2b, Slc6a4), particularly in male sham mice. Developmental sertraline exposure induces sex-specific cardiac changes, potentially affecting post-MI outcomes, with males showing more structural and survival impairments.

  PublisherOA PDFDOI

• Successful desensitization of HLA and non-HLA antibody with daratumumab-based immunotherapy: a case report from pediatric cardiac transplantation

  Human Immunology · 2025-09-01

  article
  PublisherDOI

• Impact of Magnification, Image Type, and Number on Convolutional Neural Network Performance in Differentiating Canine Large Cell Lymphoma From Non‐Lymphoma via Lymph Node Cytology

  Veterinary Clinical Pathology · 2025-09-22 · 2 citations

  articleOpen accessSenior author

  BACKGROUND: Lymph node (LN) aspirates are often obtained to distinguish large-cell lymphoma (LCL) from non-lymphoma (NL) in dogs with enlarged lymph nodes. OBJECTIVE: Images from cytology slides tested the effects of magnification, image type, and number on a convolutional neural network (CNN) differentiating canine LCL from NL. METHODS: Three hundred images of LCL and NL were used to train a CNN and interrogate the effects of image magnification, type, and number on the model's performance. Identified cases were imaged at 200×, 500×, and 1000× magnification in color and gray-scale and then used to train and identify optimal magnification and image type. The impact of the image number per cohort (50, 100, 150, 200, 250, 300) on the top model's performance was then assessed. RESULTS: The highest performance with color images was achieved at 1000× magnification, with an accuracy of 95.8%, a Receiving Operating Characteristic (ROC) area of 0.997, and an F-measure of 0.958. Similarly, the best results with gray images, also at 1000× magnification, showed an accuracy of 96.67%, a ROC area of 0.994, and an F-measure of 0.967. Performance improvements were most significant and plateaued as the number of images per class approached 150, with an accuracy of 95%, ROC area of 0.939, and F-measure of 0.95. CONCLUSION: The analysis across models suggests that color versus greyscale did not significantly impact overall performance to distinguish LCL or NL. Optimal magnification was 1000×. A minimum of 150 images per class is recommended for pilot CNN studies in this 2-class problem.

  PublisherOA PDFDOI

• METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA) BACTEREMIA AND EMPYEMA FOLLOWING TRIGGER POINT INJECTIONS (TPI)

  CHEST Journal · 2025-10-01

  article1st authorCorresponding
  PublisherDOI

• Abstract We083: A new mouse model for the study of cardiogenic TFs Tbx5, Gata4, and Mef2c during cardiogenesis

  Circulation Research · 2024-08-02

  article

  Congenital heart defects (CHDs) are be caused by mutations in genes that drive cardiac development, such as Tbx5 , Gata4 , and Mef2c . Cardiac development, and its transcriptional regulators are also regulated by microRNAs (miRs). These small RNAs target the transcripts of genes in numerous cardiac cell types during embryonic development. We and others have shown that the miR-200 family modulates the transcripts of cardiogenic transcription factors (TFs) Tbx5 , Gata4 , and Mef3c. However, the relationship between these miRs and cardiogenic TFs during in vivo cardiac development is poorly understood. During cardiogenesis, miR-200 family members are highly expressed (E14.5) but reduced in adults (3mo) (Ct Value: miR-200a : 24.3 ± 0.59 v 38.3 ± 0.21; miR-200c : 25.0 ± 0.64 v 32.5 ± 0.16). Using our miR-200 family inhibitor mice models (PMIS), we have found these miRs are required for cardiac development. PMIS-miR-200 embryos are found with a ventral septal defect and poor ventricle wall development, which is lethal by e16.5. At e14.5, PMIS-miR-200 hearts have a significant increase in expression of Tbx5, Gata4, and Mef2c compared to Wild-Type. This induced expression of these TFs is seen within CMs of the ventricle at E14.5. snMulti-Omics of WT and PMIS-miR-200 hearts found a population of CMs enriched in the PMIS-miR-200 hearts. These CMs are marked by expression of Tbx5 , Nppa , and Sox5 . RNA velocity analysis found these CMs to be “progenitor-like” and associated with an early pseudotime. Expression of Tbx5 , Nppa , and Sox5 correlated along the pseudotime with the “progenitor-like” CMs. ATAC-seq showed enrichment of Tbx5 and Mef2c motifs within this new CM cell state. Conclusions: The miR-200 family is a modulator of cardiogenic TFs expression and activity during development. Inhibition of miR-200 induces a CM cell state with “progenitor-like” qualities. Future directions will determine the role of miR- 200 in adult cardiac disease, such as ischemic injury. Our work provides new insights into gene dosage, modulated by miRs, that is required and necessary during cardiac development.

  PublisherDOI

• Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling

  American Journal of Physiology-Heart and Circulatory Physiology · 2024-10-18 · 6 citations

  articleOpen access

  Sertraline exposure during development decreased the expression of critical genes in calcium regulation and lengthened periods in calcium oscillation in neonatal cardiomyocytes. Sertraline upregulated specific microRNAs that may modulate serotonin signaling in neonatal cardiac tissues, which corresponded with a decrease in the levels of the corresponding target mRNAs. Although the echocardiograms in our adult mice suggest a mild phenotype associated with sertraline exposure, these upregulated microRNAs (miRNAs) have been linked to adult cardiovascular disease and heart failure.

  PublisherOA PDFDOI

• Persistence of Sarcocystis Neurona and Histologic Lesions in Horses with Equine Protozoal Myeloencephalitis (Epm)

  SSRN Electronic Journal · 2024-01-01 · 1 citations

  preprintOpen accessSenior author
  PublisherDOI

• Single-nuclei multiomics analysis of cardiogenic transcription factors in a new murine model of cardiac development

  Research Square · 2024-11-06

  preprintOpen access
  PublisherOA PDFDOI

Recent grants

• NIH Grant F37LM007699

  NIH · $125k · 2004

Frequent coauthors

• Robert M. Weiss

  University of Iowa

  98 shared

• Long‐Sheng Song

  University of Iowa

  70 shared

• Mark E. Anderson

  New York University

  70 shared

• William Kutschke

  University of Iowa

  67 shared

• Ang Guo

  North Dakota State University

  60 shared

• Biyi Chen

  University of Iowa

  60 shared

• Jordan D. Miller

  Mayo Clinic in Arizona

  55 shared

• Yanqi Zhu

  Gansu Provincial Hospital

  51 shared

Education

• Other

  Not specified in the provided HTML

• Ph.D.

  Not specified in the provided HTML

Awards & honors

• Diplomate, American College of Veterinary Pathologists—anato…
• Diplomate, American College of Veterinary Pathologists—clini…