About

Dr. Joshua Stern serves as the Associate Dean for Research and Graduate Studies at North Carolina State University College of Veterinary Medicine and is a Professor of Cardiology in the Department of Clinical Sciences. He earned his DVM from Ohio State University, completed his cardiology residency at NC State, and obtained a PhD in translational cardiac genetics from Washington State University. Dr. Stern is the Principal Investigator of the Stern Translational Cardiac Genetics and Pharmacogenomics Laboratory, which focuses on training clinician scientists and developing novel therapies for inherited heart disease. He is an Associate Editor for the Journal of Veterinary Internal Medicine and the current President of the Subspecialty of Cardiology in the American College of Veterinary Internal Medicine. Recognized with the 2024 AVMF Career Achievement Award in Feline Medicine, Dr. Stern is dedicated to supporting clinician scientists and training the next generation of veterinary academic leaders. With his laboratory teams, he has published over 140 peer-reviewed research manuscripts advancing the fields of companion animal genetics and translational cardiology.

Research topics

• Medicine
• Internal medicine
• Biology
• Cardiology
• Genetics
• Endocrinology
• Biochemistry
• Pharmacology
• Virology
• Animal science
• Physiology
• Intensive care medicine
• Cell biology

Selected publications

• Long-term sacubitril/valsartan is well tolerated in dogs with heart failure and myxomatous mitral valve disease and suggests excellent survival benefits

  American Journal of Veterinary Research · 2026-04-15

  articleOpen accessSenior author

  Objective: To determine the safety and survival data for dogs with congestive heart failure (CHF) and myxomatous mitral valve disease (MMVD) treated chronically with sacubitril/valsartan. Methods: A retrospective cohort study was completed by identifying dogs with CHF from MMVD and a prescription for sacubitril/valsartan over a 2.8-year period (from February 2023 to December 2025). Dogs that had surgical intervention, left atrial decompression, or an adverse event that necessitated discontinuation of sacubitril/valsartan therapy were removed from survival analysis. Results: 50 dogs with CHF and MMVD, treated with sacubitril/valsartan (mean ± SD dosage, 18.1 ± 5.4 mg/kg, PO, q 12 h) were identified. Five dogs were removed prior to survival analysis. The median survival time after the first episode of CHF was 577 days (range, 431 to 751) for 45 dogs. The survival time in 28 stage D MMVD-affected dogs, 446.5 days (283; 619), was lower than that of 17 stage C MMVD-affected dogs, who had a median survival time of 1,149 (570; infinity) days. Three dogs (6%) had adverse events, suggesting that adverse events secondary to sacubitril/valsartan were rare in this population. After initiation of sacubitril/valsartan and titration to the target dose, the most common improvements were in energy level and exercise capacity (83% of dogs). Conclusions: Sacubitril/valsartan therapy in dogs appears safe and suggests median survival times that eclipse those of prior canine MMVD stage C or D CHF studies. Clinical Relevance: This study reports a dosing schedule and clinical tolerance of sacubitril/valsartan. It further provides important data for planning future prospective studies.

  PublisherDOI

• Novel frameshift variant in exon 7 of <i>COL17A1</i> in a domestic shorthair kitten with junctional epidermolysis bullosa

  Journal of Veterinary Diagnostic Investigation · 2026-01-26

  articleOpen access

  Junctional epidermolysis bullosa (JEB) is a congenital blistering skin disorder with clefting within the lamina lucida of the basement membrane zone. We describe the clinical and morphologic features of JEB in a 4-mo-old domestic shorthair kitten and identify the underlying genetic variant. The kitten was presented with blistering lesions affecting friction-prone areas of haired skin, mucocutaneous junctions, and oral mucosa. Histopathology revealed extensive subepidermal cleft formation in affected tissues. Periodic acid–Schiff (PAS) staining showed a thin, PAS-positive line along the dermal side of the cleft, consistent with retention of the lamina densa. Transmission electron microscopy confirmed separation at the level of the lamina lucida with intact basal keratinocytes. Whole genome sequencing identified a homozygous 2-bp deletion in exon 7 of COL17A1 , predicted to result in loss of function and disrupted binding domains. Our findings support a diagnosis of JEB associated with a novel COL17A1 variant.

  PublisherOA PDFDOI

• The influence of age and captivity on cardiac structure and function in rhesus macaques

  GeroScience · 2026-04-09

  article
  PublisherDOI

• Functional toll-like receptor 4 links endotoxin sensing to platelet priming in feline platelets

  Frontiers in Veterinary Science · 2026-01-07

  articleOpen access

  Objective To characterize toll-like receptor 4 (TLR4) expression in feline platelets and to assess the priming potential of Escherichia coli lipopolysaccharide (LPS) in the presence or absence of physiologic agonists. In addition, the downstream effects of TLR4 activation on arachidonic acid (AA)-mediated signaling were investigated. Methods Eighteen healthy staff- and student-owned cats were enrolled. Washed platelets prepared from whole blood were analyzed for total and surface TLR4 expression using Western blotting, flow cytometry, and super-resolution immunofluorescence microscopy in the presence or absence of stimulation. The priming potential of LPS was evaluated by measuring alpha-granule secretion by P-selectin expression and thromboxane B 2 (TxB 2 ) generation, as a surrogate of TxA 2 , in response to adenosine diphosphate (ADP) or AA using flow cytometry and ELISA, respectively. To further examine TLR4-dependent signaling, phosphorylation of vasodilator-stimulated phosphoprotein (P-VASP) was quantified following stimulation with AA and LPS from Rhodobacter sphaeroides (LPS-RS). Results Thrombin stimulation significantly upregulated both surface and total platelet TLR4 expression. While LPS alone did not induce α-granule secretion with or without ADP, it reversed the inhibitory effect of AA by enhancing P-selectin expression and potentiating TxB 2 generation. This priming effect of LPS was mediated through TLR4, resulting in decreased cytoplasmic P-VASP, a marker associated with platelet inhibition. Discussion This study is the first to demonstrate functional TLR4 expression in feline platelets. Activation of TLR4 sensitizes platelets to AA by augmenting TxA 2 production and attenuating prostaglandin-dependent inhibitory pathways. These findings highlight a novel mechanism by which platelet TLR4 contributes to immunothrombosis and may promote thrombotic risk in cats.

  PublisherOA PDFDOI

• Evidence-Based Medical Therapy for Mitral Regurgitation in Dogs

  Preprints.org · 2026-01-28

  preprintOpen accessSenior author

  Myxomatous mitral valve disease (MMVD) is the most common acquired cardiac disease and a leading cause of congestive heart failure in dogs. Over the past three decades, experimental studies and clinical trials have established an expanding evidence base supporting pharmacologic interventions, particularly drugs that modulate hemodynamics or target the renin-angiotensin-aldosterone system (RAAS). At the same time, gaps remain in our knowledge, and several areas of clinical practice are guided more by expert consensus or extrapolation from human cardiology than by robust veterinary data. This review summarizes current evidence for pharmacologic interventions in MMVD, including established therapies such as ACE inhibitors, mineralocorticoid receptor antagonists, diuretics, and inodilators, as well as emerging drug classes such as angiotensin receptor-neprilysin inhibitors and SGLT-2 inhibitors. For each therapeutic class, we assess the strength of the available evidence, discuss methodological limitations of existing studies, and identify key gaps where additional research is needed to inform optimal clinical use.

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• Characterization of the myocardial and renal renin–angiotensin system in normal cats and cats with hypertrophic cardiomyopathy

  Journal of Veterinary Internal Medicine · 2026-05-01

  articleOpen accessSenior author

  BACKGROUND: The tissue renin-angiotensin system (RAS) has not been characterized in cats. HYPOTHESIS/OBJECTIVES: To quantify RAS enzyme activity and angiotensin peptide (AP) concentrations in myocardial and renal tissue obtained at necropsy from healthy cats and cats with hypertrophic cardiomyopathy (HCM). ANIMALS: A convenience sample of 17 adult purpose-bred cats, euthanized under other study protocols, with echocardiographically normal hearts (n = 8) or American College of Veterinary Internal Medicine stage B1 (n = 6) or C (n = 3) HCM. METHODS: Prospective study. Tissues were incubated with spiked angiotensin I (AngI) or II (AngII) under control and inhibitor conditions to assess relative enzyme contributions to AngII or angiotensin 1-7 (Ang1-7) formation. Freezing was delayed for 3 h in paired samples from 7 cats. Angiotensin peptides were also directly quantified in homogenized tissues. RESULTS: Renin-angiotensin system enzyme activity was present in necropsy tissues, which formed AngII and Ang1-7 when incubated with AP precursors. The median contribution of angiotensin-converting enzyme to AngII formation exceeded 85% in all tissues. The 90% confidence limits of the geometric mean of the ratio of the angiotensin production of paired samples met the equivalence requirement in 1/13 experiments. The AP concentrations were quantifiable and did not differ between cats with echocardiographically normal hearts and cats with HCM (myocardial AngI P = .11 and AngII P = .37; kidney AngI P = .84, AngII P = .73, and Ang 1-7 P = .84). CONCLUSIONS AND CLINICAL IMPORTANCE: Necropsy tissue RAS enzyme activity and some AP concentrations were quantifiable in this cohort. Renin-angiotensin system enzyme activity changed during a short (3 h) postmortem period.

  PublisherDOI

• Establishing a robust genetic sequencing and gene expression data library in cardiovascularly healthy cats

  Scientific Reports · 2025-07-01 · 1 citations

  articleOpen accessSenior author

  Cardiovascular disease is a leading cause of increased morbidity and mortality in cats, with hypertrophic cardiomyopathy (HCM) significantly overrepresented. While feline HCM is hereditary, the genetic etiology of disease remains poorly understood. Establishing a cohort of well-phenotyped and -genotyped healthy control cats is essential to fuel future genetic/pharmacogenetic discoveries. We sought to construct a robust genetic sequencing and gene expression library from cardiovascularly healthy cats using whole genome sequencing (WGS) and RNA sequencing (RNA-Seq). Fifty-four client-owned cats (≥ 10 years) were screened, of which 18 cats (cohort 1) were prospectively enrolled after being deemed cardiovascularly healthy by clinicopathology, biochemistry, and echocardiography. DNA isolated from blood samples was submitted for paired-end WGS at ~ 30X coverage. Standard pipelines were employed for variant calling across sequenced cats. A second cohort of 15 purpose-bred cats were euthanized for non-cardiac reasons. Flash-frozen left ventricular (LV), interventricular septum (IVS), and left atrium (LA) tissues from 11, 14, and 13 cats, respectively, were submitted for stranded mature RNA-Seq at 50 million reads/sample. Gene variants and expression profiling were catalogued for both meticulously selected cohorts. Transcriptomic and WGS data libraries were generated to serve as an open-access resource in future investigations of feline cardiovascular precision medicine.

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• Author response for "Cardiac arrhythmia prevalence and risk factors in 24-h electrocardiograms of sedentary horses"

  2025-04-12

  peer-review
  PublisherDOI

• Cardiac arrhythmia prevalence and risk factors in 24‐h electrocardiograms of sedentary horses

  Equine Veterinary Journal · 2025-07-18 · 1 citations

  articleOpen access

  BACKGROUND: Cardiac arrhythmias are common in horses, but their clinical relevance remains controversial. OBJECTIVES: To describe prevalence and identify risk factors for arrhythmias that may warrant additional screening in a sedentary mixed-breed population of horses. STUDY DESIGN: Prospective cross-sectional. METHODS: Ninety-four clinically healthy, university-owned, sedentary horses underwent 24-h ambulatory electrocardiograms and echocardiograms. Potential risk factors were recorded for all horses. Affected individuals were defined as those with >1 supraventricular premature complex/h or with any ventricular premature complexes for risk factor analysis. Forward stepwise logistic regression was used to identify factors associated with the presence of arrhythmia. The p value <0.15 was considered significant in univariable screening and p ≤ 0.05 was considered significant overall. RESULTS: During recording, 92.6% (87/94) of horses experienced an arrhythmia. Supraventricular premature complexes were present in 86.2% (81/94) of the horses, and ventricular complexes were present in 24.5% (23/94) of the horses. Of the sample, 38.3% (36/94) were considered affected by arrhythmias. Increased heart girth score was associated with detection of arrhythmias (OR 1.06, 95% CI 1-1.12, p = 0.05) and age was retained in the final model as a confounder. MAIN LIMITATIONS: The study sample included a limited range of body condition scores and number of stallions for risk factor analysis. CONCLUSION: Arrhythmias occurred with high frequency in this group of horses despite no known history or clinical signs of cardiovascular disease. Increased heart girth is a potential risk factor for arrhythmia in the horse.

  PublisherDOI

• Novel <i>Cardiac Troponin-I</i> Missense Variant (c.593C&gt;T) Is Associated With Familial Hypertrophic Cardiomyopathy in Golden Retrievers

  Circulation Genomic and Precision Medicine · 2025-08-22

  articleOpen accessSenior author

  BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a naturally occurring cardiac disorder afflicting humans, cats, rhesus macaques, pigs, and rarely dogs. The disease is characterized by maladaptive left ventricular wall thickening. Over 1500 sarcomere-coding mutations explain HCM in humans, whereas only 3 have been reported in cat breeds. To date, no mutations have been described in dogs. HCM in a nuclear family of Golden Retrievers was identified following the sudden cardiac death of 3 related puppies &lt;2 years of age from 2 dam-offspring repeat matings. METHODS: Whole-genome sequencing on the 3 affected puppies, along with nuclear family members (ie, sire, dam, 4 unaffected littermates, 4 unaffected half-siblings), and 1 distantly related, geriatric, cardiovascularly normal Golden Retriever was performed (n=14). Candidate variant genotyping was performed in an unphenotyped cohort of dogs (n=2771) and an expanded population of phenotyped, unrelated Golden Retrievers (n=45). Left ventricular tissue immunofluorescence staining was subsequently performed to investigate incorporation and expression of mutant protein within the cardiac sarcomere of HCM-affected cases. RESULTS: Gross and histopathologic evaluations of the HCM-affected puppies revealed hallmark features of the disease, including cardiomyocyte hypertrophy, interstitial fibrosis, and left-sided congestive heart failure. Segregation analysis of called variants, performed under assumptions of an autosomal-recessive mode of inheritance, identified a single segregating c.593C&gt;T missense variant in TNNI3 ( Cardiac Troponin-I ). This variant was not observed in the unphenotyped (n=2771) nor in the phenotyped, unrelated cohort of dogs (n=45). Immunofluorescence staining of left ventricular tissues did not reveal obvious aberrant protein localization and expression at the sarcomeric level, suggesting the molecular pathogenesis of the TNNI3 variant is not related to abnormal protein incorporation within the sarcomere. CONCLUSIONS: This variant represents the first-ever reported HCM-associated variant in any canine species, and its identification holds promise for establishing translational models, genetic screening, and early disease prevention within the breed.

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Frequent coauthors

• Kathryn M. Meurs

  North Carolina State University

  48 shared

• Victor N. Rivas

  North Carolina State University

  34 shared

• Yu Ueda

  33 shared

• Joanna L. Kaplan

  University of California, Davis

  27 shared

• Ronald H. L. Li

  26 shared

• Maureen S. Oldach

  University of California, Davis

  25 shared

• Lance C. Visser

  Colorado State University

  24 shared

• Eric S. Ontiveros

  Children’s Institute

  23 shared

Labs

• Stern Translational Cardiac Genetics and Pharmacogenomics LaboratoryPI

Education

• Ph.D., Animal Science

  University of California, Davis

  2003

• M.S., Animal Science

  University of California, Davis

  1999

• B.S., Animal Science

  University of California, Davis

  1997

Awards & honors

• 2024 AVMF Career Achievement Award in Feline Medicine