About

Alexia Vite, PhD, is a Research Assistant Professor of Medicine in the Department of Cardiovascular Medicine at the University of Pennsylvania School of Medicine. Her expertise encompasses cardiac myocyte biology and genetic cardiomyopathies, with extensive experience in studying the consequences of mutations causing inherited cardiomyopathies, cardiovascular development and physiology, tissue engineering, cell physiology, stem cells, and human tissue research. Her current research focuses on identifying the causes of reduced glucose utilization in the context of insulin resistance, aiming to develop strategies to prevent energy starvation that contributes to the progression of cardiomyopathies. This multi-component project investigates the role of mechanical stress in insulin resistance and glucose utilization impairment in adult cardiomyocytes and cardiac tissues, employing a combination of bioengineering and molecular biology techniques.

Research topics

• Biology
• Medicine
• Chemistry
• Internal medicine
• Endocrinology
• Cell biology
• Biochemistry

Selected publications

• 26-A-14618-ACC METFORMIN MITIGATES EXTRACELLULAR STIFFNESS-INDUCED CONTRACTILE FATIGUE IN CARDIOMYOCYTES

  Journal of the American College of Cardiology · 2026-03-27

  article
  PublisherDOI

• T-tubular remodeling occurs in a cardiomyocyte-autonomous manner following pathological mechanical stiffness exposure

  Journal of Molecular and Cellular Cardiology Plus · 2026-03-23

  articleOpen access

  -release dyssynchrony, and disrupted T-tubule organization, causing a shift from transverse to longitudinal orientation. We found no differences in key T-tubule total protein levels between experimental groups but observed spatial reorganization of TCAP in response to substrate stiffening. Microtubule depolymerization with nocodazole prevented pathological t-tubule remodeling, suggesting that microtubules act as mechanotransducers that orchestrate subcellular reorganization in response to mechanical cues. Our findings highlight the intrinsic ability of cardiomyocytes to remodel in response to mechanical load in the form of extracellular mechanical stiffness, in the absence of external hormonal influences, other cell types, the extracellular matrix, and other compensatory systemic responses, and that this is largely mediated by the microtubular network.

  PublisherDOI

• Effect of Metformin On Living Myocardial Slices Ventricular Function and Glucose Uptake

  ScholarlyCommons (University of Pennsylvania) · 2026-04-09

  other

  Heart failure (HF) is characterized by impaired cardiac function and decreased myocardial metabolism. Metformin, a common treatment for type 2 diabetes, has been shown to activate AMP-activated protein kinase (AMPK), which promotes translocation of the glucose transporter GLUT4 to the cardiomyocyte membrane. This study investigates the effects of metformin on ventricular mechanical function and substrate (glucose, fatty acids) uptake in living myocardial slices (LMS). Rat ventricular LMS were prepared and fatigued under two afterload conditions (25% and 75% afterload). Slices were treated with 0.2 mM metformin or left untreated as controls. Mechanical work was assessed using a cardiac slice system before and after 15 min of fatigue procedure. Glucose uptake was evaluated using 2-NBDG fluorescence, and fatty acid uptake was assessed via fluorescent labeling. Metformin treatment significantly increased glucose uptake in LMS at 25% afterload compared to the control, shown by elevated 2-NBDG fluorescence intensity. This effect was not observed at 75% afterload. Additionally, metformin improved mechanical work of LMS prior to fatigue under both afterload conditions; however, these improvements diminished after the fatigue. Fatty acid uptake showed no consistent enhancement with metformin treatment. These findings suggest that metformin treatment increases glucose uptake of LMS and improves contractile performance in myocardial tissue under lower afterload conditions, likely through AMPK-mediated GLUT4 translocation. The diminished effects at higher afterload and after the fatigue procedure shows potential limitations of metformin.

  Publisher

• Mechanisms driving mechanical memory in adult rat and human Cardiomyocytes

  Journal of Molecular and Cellular Cardiology Plus · 2025-06-01

  articleOpen access
  PublisherDOI

• Mechanical Load Induces Insulin Resistance in Adult Cardiomyocytes via Cell Autonomous and Microtubule-Dependent Mechanisms

  Journal of Molecular and Cellular Cardiology Plus · 2025-06-01

  articleOpen access1st authorCorresponding
  PublisherDOI

• Micropatterned Magneto-Rheological Elastomers to Drive Changes in Cardiomyocyte Alignment

  Journal of Visualized Experiments · 2025-06-10 · 1 citations

  article

  Substrate-associated cues, such as mechanical and topographic, profoundly influence cellular response. However, much of the foundational research employs static or isolated effects. The direction and timescale of these mechanical effects on emergent cellular responses remain largely unexplored. Tools to examine how time-varying substrate-associated stimuli drive physiological and pathological processes can unlock the next level of mechanobiological insight. Here, we use micro-patterned magnetorheological elastomers (MREs) that can rapidly stiffen and soften in response to an external magnetic field, allowing for a more rigorous investigation of the effects of mechanical (stiffness) and contact-guided (topographic) stimulation on neonatal rat cardiomyocyte orientation and alignment. By integrating dynamic control of mechanical stiffness that can be temporally tuned and reversed, we can rigorously test the effects of load by (1) pre-conditioning under identical conditions and (2) acutely changing in vitro biomechanics to mimic clinically relevant phenomenology, such as myocardial infarction properly. This approach allows us to study the impact of load on cellular responses in a more realistic and controlled manner.

  PublisherDOI

• A Dynamic Gradient Stiffness Material Platform to Manipulate Cardiac Fibroblasts' Spatio‐Temporal Behavior

  Advanced Functional Materials · 2024-04-05 · 6 citations

  articleOpen access

  Abstract After myocardial infarction, there exists a spatiotemporal variation of cardiac tissue stiffness across the infarcted border region outward to remote regions, influencing adverse remodeling and cardiac fibrosis, and this stiffness gradient changes over time. Here, a platform with dynamic, tunable, and reversible gradient stiffness can recapitulate in vitro the time‐dependent stiffness range across the infarction border that occurs as part of the remodeling process is presented. This platform enables the observation of time‐dependent interaction between cardiac fibroblasts and their mechanical microenvironment in a spatiotemporal manner. Specifically, the competition and cooperation of a chemical cue (antifibrotic drug) and mechanical cue (gradient softening) in tandem to attenuate the fibrotic responses of cardiac fibroblasts is examined. Applying a combined intervention showed either additive or antagonistic effects on fibrosis‐related gene regulation compared to separate interventions of drug or softening. This work reveals the spatiotemporal variation of fibrotic response in cardiac fibroblasts as well as the complexity of antifibrotic drug dosing with stiffness changes and their combinatory effect on cardiac fibroblasts. This platform provides a unique in vitro tool to study disease progression mechanisms in a more clinically relevant microenvironment and also serves as a cost‐effective model for potential therapeutic screening.

  PublisherOA PDFDOI

• Distinct cytoskeletal regulators of mechanical memory in cardiac fibroblasts and cardiomyocytes

  Basic Research in Cardiology · 2024-02-13 · 11 citations

  article
  PublisherDOI

• Vasohibin inhibition improves myocardial relaxation in a rat model of heart failure with preserved ejection fraction

  Science Translational Medicine · 2024-07-17 · 21 citations

  article

  Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome associated with increased myocardial stiffness and cardiac filling abnormalities. Prior studies implicated increased α-tubulin detyrosination, which is catalyzed by the vasohibin enzymes, as a contributor to increased stabilization of the cardiomyocyte microtubule network (MTN) and stiffness in failing human hearts. We explored whether increased MTN detyrosination contributed to impaired diastolic function in the ZSF1 obese rat model of HFpEF and designed a small-molecule vasohibin inhibitor to ablate MTN detyrosination in vivo. Compared with ZSF1 lean and Wistar Kyoto rats, obese rats exhibited increased tubulin detyrosination concomitant with diastolic dysfunction, left atrial enlargement, and cardiac hypertrophy with a preserved left ventricle ejection fraction, consistent with an HFpEF phenotype. Ex vivo myocardial phenotyping assessed cardiomyocyte mechanics and contractility. Vasohibin inhibitor treatment of isolated cardiomyocytes from obese rats resulted in reduced stiffness and faster relaxation. Acute in vivo treatment with vasohibin inhibitor improved diastolic relaxation in ZSF1 obese rats compared with ZSF1 lean and Wistar Kyoto rats. Vasohibin inhibition also improved relaxation in isolated human cardiomyocytes from both failing and nonfailing hearts. Our data suggest the therapeutic potential for vasohibin inhibition to reduce myocardial stiffness and improve relaxation in HFpEF.

  PublisherDOI

• Functional Impact of Alternative Metabolic Substrates in Failing Human Cardiomyocytes

  JACC Basic to Translational Science · 2023-09-20 · 15 citations

  articleOpen access1st author

  Recent studies suggest that metabolic dysregulation in patients with heart failure might contribute to myocardial contractile dysfunction. To understand the correlation between function and energy metabolism, we studied the impact of different fuel substrates on human nonfailing or failing cardiomyocytes. Consistent with the concept of metabolic flexibility, nonfailing myocytes exhibited excellent contractility in all fuels provided. However, impaired contractility was observed in failing myocytes when carbohydrates alone were used but was improved when additional substrates were added. This study demonstrates the functional significance of fuel utilization shifts in failing human cardiomyocytes.

  PublisherDOI

Frequent coauthors

• Philippe Charron

  Inserm

  60 shared

• Estelle Gandjbakhch

  57 shared

• Glenn L. Radice

  Brown University

  52 shared

• Jifen Li

  Translational Therapeutics (United States)

  50 shared

• Roslyn Yi

  Bluebird Bio (United States)

  50 shared

• Ludovic Gomez

  Université Claude Bernard Lyon 1

  49 shared

• Erhe Gao

  Temple University

  49 shared

• Frans van Roy

  Cancer Research Institute Ghent

  49 shared

Education

• Ph.D.

  Pierre et Marie Curie University

  2013

• Other, Physiology/Physiopathology

  Pierre et Marie Curie University

  2009