Jil Tardiff

About

Jil Tardiff, MD, PhD, is a professor of medicine and cellular and molecular medicine at the University of Arizona College of Medicine - Tucson. She is also a member of the Clinical and Translational Institute at the BIO5 Institute. Her academic background includes a BA in genetics from the University of California at Berkeley, and both an MD and a PhD in cell biology from the Albert Einstein College of Medicine. Her training includes house staff training at Columbia-Presbyterian Medical Center and participation in the ABIM Clinician-Scientist pathway, completing an internal medicine residency and a combined clinical-research fellowship in cardiovascular medicine. Her research focuses on the mechanisms underlying the development of hypertrophic cardiomyopathy (HCM), the most common form of genetic cardiomyopathy caused by mutations in proteins of the cardiac sarcomere. Her work investigates disease pathogenesis at the cellular level using transgenic mouse models and has been continuously funded by the NIH since 2001. Her studies have contributed to understanding how mutations cause this complex disorder and have supported the development of new clinical trials for treatment. In collaboration with other researchers, her lab has developed computational approaches to model and predict disease severity based on protein structure. Her goal is to establish an HCM Center of Excellence at the University of Arizona to provide lifelong, cutting-edge care for patients affected by this…

Research topics

• Bioinformatics
• Biology
• Medicine
• Pathology
• Genetics
• Neuroscience
• Computational biology
• Immunology
• Cardiology
• Pharmacology

Selected publications

• Myosin modulators: emerging approaches for the treatment of cardiomyopathies and heart failure

  Journal of Clinical Investigation · 2022 · 64 citations

  Myosin modulators are a novel class of pharmaceutical agents that are being developed to treat patients with a range of cardiomyopathies. The therapeutic goal of these drugs is to target cardiac myosins directly to modulate contractility and cardiac power output to alleviate symptoms that lead to heart failure and arrhythmias, without altering calcium signaling. In this Review, we discuss two classes of drugs that have been developed to either activate (omecamtiv mecarbil) or inhibit (mavacamten…

  DOI

• Complexity in genetic cardiomyopathies and new approaches for mechanism-based precision medicine

  The Journal of General Physiology · 2021 · 40 citations

  Senior authorCorresponding

  Genetic cardiomyopathies have been studied for decades, and it has become increasingly clear that these progressive diseases are more complex than originally thought. These complexities can be seen both in the molecular etiologies of these disorders and in the clinical phenotypes observed in patients. While these disorders can be caused by mutations in cardiac genes, including ones encoding sarcomeric proteins, the disease presentation varies depending on the patient mutation, where mutations ev…

  DOI

• Empagliflozin enhances metabolic efficiency and improves left ventricular hypertrophy in a hypertrophic cardiomyopathy mouse model

  European Heart Journal · 2025-04-30 · 9 citations

  articleOpen access

  BACKGROUND AND AIMS: Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and impaired metabolic efficiency. This study investigates the therapeutic potential of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) empagliflozin (EMPA) in ameliorating these pathological features in a mouse model carrying the myosin R403Q mutation. METHODS: Male mice harbouring the R403Q mutation were treated with EMPA for 16…

  PublisherDOI

• A rare splice-site variant in <i>TNNT2</i>: the need for ancestral diversity in genomic reference data sets

  European Heart Journal · 2025-03-05 · 4 citations

  articleOpen access
  PublisherOA PDFDOI

• A rare splice-site variant in cardiac troponin-T ( <i>TNNT2)</i> : The need for ancestral diversity in genomic reference datasets

  medRxiv · 2024-02-11 · 3 citations

  preprintOpen access

  ABSTRACT The underrepresentation of different ancestry groups in large genomic datasets creates difficulties in interpreting the pathogenicity of monogenic variants. Genetic testing for individuals with non-European ancestry results in higher rates of uncertain variants and a greater risk of misclassification. We report a rare variant in the cardiac troponin T gene, TNNT2 ; NM_001001430.3: c.571-1G&gt;A (rs483352835) identified via research-based whole exome sequencing in two unrelated probands…

  PublisherOA PDFDOI

Recent grants

• NIH Grant K08HL068619

  NIH · $657k · 2007

• Emerging Opportunities in Cardiovascular Disease

  NIH · $10k · 2020–2021

• A New Paradigm to Incorporate Protein Dynamics into Targeted Small Molecule Design for Sarcomeric Cardiomyopathies: A Proof of Concept for Thin Filament Therapeutics

  NIH · $1.9M · 2018–2022

Frequent coauthors

• Steven D. Schwartz

  University of Arizona

  63 shared

• Jolanda van der Velden

  Vrije Universiteit Amsterdam

  43 shared

• Pieter P. de Tombe

  Inserm

  39 shared

• Melissa L. Lynn

  University of Arizona

  37 shared

• Karin R. Sipido

  KU Leuven

  36 shared

• Ilkka Heinonen

  Turku PET Centre

  36 shared

• David Eisner

  Manchester Academic Health Science Centre

  36 shared

• Rob Wu

  Amsterdam UMC Location VUmc

  36 shared

Awards & honors

• Steven M. Gootter Endowed Chair for the Prevention of Sudden…

Similar researchers at University of Arizona

• Mark Van Dykeh-55
• Philipp Gutrufh-49
• Urs Utzingerh-37