Eldorado Hotel & Spa Floorplan
This meeting took place in 2023
For a complete list of the meetings for the upcoming/current season, see our meeting list, or search for a meeting.
Heart Failure: All Cells Considered (Z7)
Organizer(s) Merry L. Lindsey, Crystal Ripplinger and Zamaneh Kassiri
June 25—28, 2023
Eldorado Hotel & Spa • Santa Fe, NM USA
Abstract Deadline: Apr 19, 2023
Scholarship Deadline: Apr 19, 2023
Discounted Registration Deadline: Apr 25, 2023
Sponsored by AstraZeneca, Ionis Pharmaceuticals, Inc., Merck & Co., Inc. and Novo Nordisk A/S
Summary of Meeting:
Heart failure (HF) has conventionally been defined as the inability of the heart to pump sufficiently to meet the needs of the body for oxygen. In addition to HF with reduced ejection fraction (HFrEF), nearly half of patients who present with HF signs and symptoms have preserved ejection fraction (HFpEF). HFrEF presentation includes reduced contractile function and dilation of the left ventricle (LV), while HFpEF presentation includes abnormal LV relaxation and diastolic stiffness. Both HF types have similar hospitalization, morbidity, and mortality rates, and medications that improve outcomes for patients with HFrEF do not show similar benefit to patients with HFpEF. Understanding the cell signaling pathways and molecular mechanisms that trigger HF is a major challenge in cardiovascular medicine. Our conference is conceptually framed around the hypothesis that while HFrEF and HFpEF clearly have distinct etiologies and driving mechanisms, they may share modifiable pathways and biological mediators in common. The convergence among cells involved in inflammation and extracellular matrix deposition will be a major theme. The meeting program includes specific focus on cell heterogeneity, cell-cell cross-talk, individual cell responses, cardiac interactions with other organs, cardiometabolic aspects of all cell types, and approaches to identify new pharma targets. Scientific Relevance: There is a strong need to better understand the cellular and molecular mechanisms of heart failure development. Gaps: 1. Clarify concepts of cardiac remodeling, inflammation, fibrosis, and cell heterogeneity. 2. Develop standard procedures for rigorous assessments. 3. Examine exacerbation of HF development in the setting of co-morbidities. 4. Harness knowledge from other research arenas to develop new strategies to combat HF. 5. Define the use of animal models for optimal use in HF research. 6. Define phenotypes that distinguish subtypes of heart failure (HF): HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Specific Aims: 1. to disseminate and share new knowledge about heart failure, focused on cell and molecular signaling that yields HF; 2. to focus on controversies and knowledge gaps that prevent or limit therapeutic translation; and 3. to promote the educational growth and careers of young scientists. Anticipated outcomes: 1. Attendees will leave this meeting with clear ideas on the most critical experiments needed to accelerate the field forward. 2. There will be a better understanding of the methods that can be applied to better translate basic science to clinical use. 3. Trainees will understand how to advance their careers in the heart failure field. 4. Scientific knowledge and clinical practice will be advanced in that we will have a comprehensive evaluation of the current state of understanding of heart failure and better understand the challenges that remain before we can more completely translate the dynamics of cellular interactions in heart failure. Innovation: We know of no other conference that focuses on the cellular components of heart failure. We will challenge current concepts and fill in the knowledge gaps to help propel the field forward. Bringing together interdisciplinary groups of investigators will ample provide opportunity for cross-fertilization. In particular, we will use approaches in proteomics and big data science to seek paradigm shifts in research strategies.
View Scholarships/Awards
Heart failure (HF) has conventionally been defined as the inability of the heart to pump sufficiently to meet the needs of the body for oxygen. In addition to HF with reduced ejection fraction (HFrEF), nearly half of patients who present with HF signs and symptoms have preserved ejection fraction (HFpEF). HFrEF presentation includes reduced contractile function and dilation of the left ventricle (LV), while HFpEF presentation includes abnormal LV relaxation and diastolic stiffness. Both HF types have similar hospitalization, morbidity, and mortality rates, and medications that improve outcomes for patients with HFrEF do not show similar benefit to patients with HFpEF. Understanding the cell signaling pathways and molecular mechanisms that trigger HF is a major challenge in cardiovascular medicine. Our conference is conceptually framed around the hypothesis that while HFrEF and HFpEF clearly have distinct etiologies and driving mechanisms, they may share modifiable pathways and biological mediators in common. The convergence among cells involved in inflammation and extracellular matrix deposition will be a major theme. The meeting program includes specific focus on cell heterogeneity, cell-cell cross-talk, individual cell responses, cardiac interactions with other organs, cardiometabolic aspects of all cell types, and approaches to identify new pharma targets. Scientific Relevance: There is a strong need to better understand the cellular and molecular mechanisms of heart failure development. Gaps: 1. Clarify concepts of cardiac remodeling, inflammation, fibrosis, and cell heterogeneity. 2. Develop standard procedures for rigorous assessments. 3. Examine exacerbation of HF development in the setting of co-morbidities. 4. Harness knowledge from other research arenas to develop new strategies to combat HF. 5. Define the use of animal models for optimal use in HF research. 6. Define phenotypes that distinguish subtypes of heart failure (HF): HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Specific Aims: 1. to disseminate and share new knowledge about heart failure, focused on cell and molecular signaling that yields HF; 2. to focus on controversies and knowledge gaps that prevent or limit therapeutic translation; and 3. to promote the educational growth and careers of young scientists. Anticipated outcomes: 1. Attendees will leave this meeting with clear ideas on the most critical experiments needed to accelerate the field forward. 2. There will be a better understanding of the methods that can be applied to better translate basic science to clinical use. 3. Trainees will understand how to advance their careers in the heart failure field. 4. Scientific knowledge and clinical practice will be advanced in that we will have a comprehensive evaluation of the current state of understanding of heart failure and better understand the challenges that remain before we can more completely translate the dynamics of cellular interactions in heart failure. Innovation: We know of no other conference that focuses on the cellular components of heart failure. We will challenge current concepts and fill in the knowledge gaps to help propel the field forward. Bringing together interdisciplinary groups of investigators will ample provide opportunity for cross-fertilization. In particular, we will use approaches in proteomics and big data science to seek paradigm shifts in research strategies.
View Scholarships/Awards
No registration fees are used to fund entertainment or alcohol at this conference
The meeting will begin on Sunday, June 25 with registration from 16:00 to 20:00 and a welcome mixer from 18:00 to 20:00. Conference events conclude on Wednesday, June 28 with a closing plenary session from 17:00 to 19:00, followed by a social hour. We recommend return travel on Thursday, June 29 in order to fully experience the meeting.
SUNDAY, JUNE 25
MONDAY, JUNE 26
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
TUESDAY, JUNE 27
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
WEDNESDAY, JUNE 28
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
THURSDAY, JUNE 29
Conference Program Print | View meeting in 24 hr (international) time
The meeting will begin on Sunday, June 25 with registration from 16:00 to 20:00 and a welcome mixer from 18:00 to 20:00. Conference events conclude on Wednesday, June 28 with a closing plenary session from 17:00 to 19:00, followed by a social hour. We recommend return travel on Thursday, June 29 in order to fully experience the meeting.
SUNDAY, JUNE 25
6:00—8:00 PM
Welcome Mixer
No registration fees are used to fund alcohol served at this function.
8:00—9:00 AM
Welcome and Keynote Address (Joint)
*
Merry L. Lindsey,
Meharry Medical Center, USA
*
Marlene Rabinovitch,
Stanford University, USA
Elizabeth M. McNally,
Northwestern University, USA
Genetic Determinants of Heart Failure
Genetic Determinants of Heart Failure
9:30—11:15 AM
Cell-Cell Cross-Talk
*
Merry L. Lindsey,
Meharry Medical Center, USA
*
Upendra Chalise,
University of Nebraska Medical Center, USA
Gillian A. Gray,
University of Edinburgh Centre for Cardiovascular Science, UK
Intracellular Glucocorticoid Regeneration as a Novel Target to Regulate Infarct Repair and Progression to Heart Failure
Intracellular Glucocorticoid Regeneration as a Novel Target to Regulate Infarct Repair and Progression to Heart Failure
Karin Sipido,
KU Leuven, Belgium
Cellular Cross-talk in Ischemic Cardiomyopathy
Cellular Cross-talk in Ischemic Cardiomyopathy
Jennifer E. Van Eyk,
Cedars-Sinai, USA
Harnessing Proteomics for Novel HF Diagnostics and Therapies
Harnessing Proteomics for Novel HF Diagnostics and Therapies
Jason Maynes,
Hospital for Sick Children, Canada
Short Talk: Inherent Inflammatory Characteristics Determine Repair and Transferable Benefit of Cardiac Progenitor Cells in Patients with Congenital Heart Disease
Short Talk: Inherent Inflammatory Characteristics Determine Repair and Transferable Benefit of Cardiac Progenitor Cells in Patients with Congenital Heart Disease
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
9:30—11:30 AM
The Metabolic Basis of Pulmonary Arterial Hypertension Beyond Glycolysis
*
John Shyy,
University of California, USA
*
David Fulton,
Augusta University, USA
Marlene Rabinovitch,
Stanford University, USA
Integrating Pathways in Pulmonary Hypertension
Integrating Pathways in Pulmonary Hypertension
Sadis Matalon,
University of Alabama at Birmingham, USA
Oxidative Mitochondrial DNA Injury is a Key Contributor to the Development of Chemical Lung Injury
Oxidative Mitochondrial DNA Injury is a Key Contributor to the Development of Chemical Lung Injury
Stephen L. Archer,
Queen's University, Canada
The Role of Altered Mitochondrial Dynamics and Metabolism in Pulmonary Hypertension
The Role of Altered Mitochondrial Dynamics and Metabolism in Pulmonary Hypertension
Michela Noseda,
Imperial College London, UK
Single Cell and Spatial Transcriptomics State-of-the-heart
Single Cell and Spatial Transcriptomics State-of-the-heart
2:30—4:30 PM
Workshop 1
*
Nicholas W. Chavkin,
University of Virginia, USA
*
Mikito Takefuji,
Nagoya University School of Medicine, Japan
Preethy Parthiban,
University of Minnesota- Twin Cities, USA
Macrophage-derived CCL24 Worsens Cardiac Dysfunction by Promoting Fibrosis and Impeding Compensatory Adaptation during Heart Failure
Macrophage-derived CCL24 Worsens Cardiac Dysfunction by Promoting Fibrosis and Impeding Compensatory Adaptation during Heart Failure
Upendra Chalise,
University of Nebraska Medical Center, USA
Big Data Guided Analysis Reveals Unique Cardiac Remodeling Trajectories by Sex After Myocardial Infarction
Big Data Guided Analysis Reveals Unique Cardiac Remodeling Trajectories by Sex After Myocardial Infarction
Benjamin D. McNair,
University of Wyoming, USA
Distinct Mechanisms of Aging in the Right and Left Ventricles
Distinct Mechanisms of Aging in the Right and Left Ventricles
Bryana N. Harris,
University of Virginia, USA
Dynamic Map Illuminates Hippo Module Crosstalk Driving Cardiomyocyte Proliferation
Dynamic Map Illuminates Hippo Module Crosstalk Driving Cardiomyocyte Proliferation
Karin J. Bosma,
Vanderbilt University Medical Center, USA
Modulation of Prostaglandin E2 Receptors EP3 and EP4 as a Novel Therapeutic Strategy to Improve Cardiac Function in Type 2 Diabetes
Modulation of Prostaglandin E2 Receptors EP3 and EP4 as a Novel Therapeutic Strategy to Improve Cardiac Function in Type 2 Diabetes
Alexa Corker,
Medical University of South Carolina, USA
PTSD has a Negative Impact on Cardiac Homeostasis
PTSD has a Negative Impact on Cardiac Homeostasis
Abraham L. Bayer,
Tufts Graduate School of Biomedical Sciences, USA
T-Cell MyD88 is a Novel Regulator of Cardiac Fibrosis through Modulation of T-cell Activation
T-Cell MyD88 is a Novel Regulator of Cardiac Fibrosis through Modulation of T-cell Activation
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
2:30—4:30 PM
Workshop 1: Imaging and Biomarkers of Disease Altering Therapies
*
Christopher Rhodes,
Imperial College London, UK
S M Riajul Wahab,
University of Texas at El Paso, USA
Identifying the Role of Prion-like Protein Doppel as a Novel Mediator of Pulmonary Arterial Hypertension
Identifying the Role of Prion-like Protein Doppel as a Novel Mediator of Pulmonary Arterial Hypertension
Claudia Mickael,
University of Colorado Denver, USA
Classical Dendritic Cells Drive and Maintain Hypoxia-Induced Pulmonary Hypertension
Classical Dendritic Cells Drive and Maintain Hypoxia-Induced Pulmonary Hypertension
Micheala A. Aldred,
Indiana University, USA
Cybrid Analysis Delineates Nuclear and Mitochondrial Contributions to Oxidative Stress in Pulmonary Arterial Hypertension
Cybrid Analysis Delineates Nuclear and Mitochondrial Contributions to Oxidative Stress in Pulmonary Arterial Hypertension
Cassidy Delaney,
University of Colorado, USA
Platelets Participate in Regulation of the Early Immune Response in Experimental PH
Platelets Participate in Regulation of the Early Immune Response in Experimental PH
Slaven Crnkovic,
Medical University of Graz, Austria
Defining Cell-type Specific Disease States in Pulmonary Hypertension
Defining Cell-type Specific Disease States in Pulmonary Hypertension
Jingbo Dai,
Northwestern University, USA
The RNA m6A Demethylase, FTO, Regulates Vascular Remodeling in the Pathogenesis of Pulmonary Arterial Hypertension
The RNA m6A Demethylase, FTO, Regulates Vascular Remodeling in the Pathogenesis of Pulmonary Arterial Hypertension
Bin Liu,
University of Arizona, USA
Fatty Acid-binding Proteins Promote Pulmonary Arterial Hypertension via Glycolysis
Fatty Acid-binding Proteins Promote Pulmonary Arterial Hypertension via Glycolysis
Caitlin Lewis,
University of Colorado, USA
Extracellular Superoxide Dismutase Affects Interstitial Macrophage Accumulation, Reprogramming and Hyaluronan Binding during Pulmonary Hypertension
Extracellular Superoxide Dismutase Affects Interstitial Macrophage Accumulation, Reprogramming and Hyaluronan Binding during Pulmonary Hypertension
5:00—7:00 PM
Cell Heterogeneity in Heart Failure
*
Gillian A. Gray,
University of Edinburgh Centre for Cardiovascular Science, UK
*
Preethy Parthiban,
University of Minnesota- Twin Cities, USA
Amy D. Bradshaw,
Medical University of South Carolina, USA
Fibroblast Activation Profiles in Pressure Overload
Fibroblast Activation Profiles in Pressure Overload
Jennifer Davis,
University of Washington, USA
Mechanical Signaling Networks that Program Fibroblasts
Mechanical Signaling Networks that Program Fibroblasts
Taben Hale,
University of Arizona, USA
Sub-Populations of Resident Cardiac Fibroblasts in Hypertension: Taking a Census
Sub-Populations of Resident Cardiac Fibroblasts in Hypertension: Taking a Census
Alessandra Pasut,
KULeuven, Belgium
Short Talk: Metabolic Heterogeneity of Endothelial Cells in HFpEF
Short Talk: Metabolic Heterogeneity of Endothelial Cells in HFpEF
Richard Keith Babbs,
Keros Therapeutics, USA
Short Talk: RKER-012, A Novel Modified ActRIIB Ligand Trap, Attenuated Cardiac Hypertrophy, Fibrosis, and Cardiovascular Remodeling in a Transaortic Constriction Model of Heart Failure
Short Talk: RKER-012, A Novel Modified ActRIIB Ligand Trap, Attenuated Cardiac Hypertrophy, Fibrosis, and Cardiovascular Remodeling in a Transaortic Constriction Model of Heart Failure
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
5:00—7:00 PM
How Epigenetic Changes and RNA Translation Govern Disease Susceptibility
*
Ke Yuan,
Boston Children's Hospital, USA
*
Scott Barman,
Augusta University, USA
Sebastien Bonnet,
Université Laval, Canada
Epigenetics Targets in PAH: BRD4 and ACLY Novel's Targets for Vascular Remodeling
Epigenetics Targets in PAH: BRD4 and ACLY Novel's Targets for Vascular Remodeling
Soni Savai Pullamsetti,
Max-Planck-Institute for Heart and Lung Research, Germany
The Suppressor Function of lnc RNAs in Pulmonary Hypertension
The Suppressor Function of lnc RNAs in Pulmonary Hypertension
Chen-Shan Julia Woodcock,
University of Pittsburgh, USA
Short Talk: RNA Editing Deficiency Induces Pulmonary Endothelial Pathophenotypes and Drives Pulmonary Hypertension
Short Talk: RNA Editing Deficiency Induces Pulmonary Endothelial Pathophenotypes and Drives Pulmonary Hypertension
Cheng-Jun Hu,
University of Colorado Denver, USA
Short Talk: Pulmonary Vascular Fibroblasts Are Epigenetically Primed for Inflammatory Responses
Short Talk: Pulmonary Vascular Fibroblasts Are Epigenetically Primed for Inflammatory Responses
YouYang Zhao,
Northwestern University-Lurie Children's Hospital of Chicago, USA
Short Talk: Endothelial Cell-targeted Nanoparticle Delivery of CRISPR/Cas9 Plasmid DNA Disrupts Endothelial HIF-2a in Adult Rats and Inhibits Experimental PAH: Towards Genome Editing Therapy of PAH
Short Talk: Endothelial Cell-targeted Nanoparticle Delivery of CRISPR/Cas9 Plasmid DNA Disrupts Endothelial HIF-2a in Adult Rats and Inhibits Experimental PAH: Towards Genome Editing Therapy of PAH
Jingbo Dai,
Northwestern University, USA
Short Talk: Therapeutic Genome Editing of Endothelial Fabp4 Inhibits Pulmonary Arterial Hypertension in Rats
Short Talk: Therapeutic Genome Editing of Endothelial Fabp4 Inhibits Pulmonary Arterial Hypertension in Rats
7:00—8:00 PM
Social Hour with Lite Bites
No registration fees are used to fund alcohol served at this function.
8:00—11:00 AM
Cardiopulmonary Crossroads (Joint)
*
Zamaneh Kassiri,
University of Alberta, Canada
*
Gaurav Choudhary,
Alpert Medical School of Brown University, USA
Tim Lahm,
National Jewish Health, USA
Sex as a Determinant of Right Ventricular Dysfunction in Pulmonary Hypertension
Sex as a Determinant of Right Ventricular Dysfunction in Pulmonary Hypertension
Tami Martino,
University of Guelph, Canada
Circadian Rhythms and HF Chronotherapy
Circadian Rhythms and HF Chronotherapy
Coffee Break
Bradley Maron,
University of Maryland School of Medicine, USA
Individualized Interactomes Advance Precision Medicine in Heart Failure Syndromes
Individualized Interactomes Advance Precision Medicine in Heart Failure Syndromes
Crystal Ripplinger,
University of California, Davis, USA
The Nervous Heart: Autonomic Remodeling Post-MI
The Nervous Heart: Autonomic Remodeling Post-MI
Yongneng Zhang,
University of Alberta, Canada
Short Talk: A Critical Contribution of Cardiac Myofibroblasts in RV Failure and the Role of a UCP2 SNP as a Biomarker Identifying PAH Patients Predisposed to RV Decompensation
Short Talk: A Critical Contribution of Cardiac Myofibroblasts in RV Failure and the Role of a UCP2 SNP as a Biomarker Identifying PAH Patients Predisposed to RV Decompensation
Kenzo Ichimura,
Stanford University, USA
Short Talk: 3D Deep Tissue Imaging Reveals Complex Remodeling of the Microvasculature in Right Heart Failure
Short Talk: 3D Deep Tissue Imaging Reveals Complex Remodeling of the Microvasculature in Right Heart Failure
3:00—4:30 PM
Workshop 2
*
Thomas Martin,
University of Colorado Boulder, USA
*
Alexa Corker,
Medical University of South Carolina, USA
Thirupura Sundari Shankar,
University of Utah, USA
Adipocyte Enhancer Binding Protein 1 as a Novel Therapeutic Target to Combat Fibrosis in Heart Failure
Adipocyte Enhancer Binding Protein 1 as a Novel Therapeutic Target to Combat Fibrosis in Heart Failure
Mikito Takefuji,
Nagoya University School of Medicine, Japan
Cardiac Atypical Kinase Improves Left Ventricular Diastolic Dysfunction in Heart Failure with Preserved Ejection Fraction
Cardiac Atypical Kinase Improves Left Ventricular Diastolic Dysfunction in Heart Failure with Preserved Ejection Fraction
Mohit Kumar,
Regeneron Pharmaceuticals, Inc., USA
Characterization of Right Ventricle Involvement in MYBPC3-linked Hypertrophic Cardiomyopathy
Characterization of Right Ventricle Involvement in MYBPC3-linked Hypertrophic Cardiomyopathy
Patricia Perez-Bonilla,
Pfizer Inc., USA
Heart Rate Variability and Chronotropic Incompetence as Prognostic Markers in a HFpEF Preclinical Model
Heart Rate Variability and Chronotropic Incompetence as Prognostic Markers in a HFpEF Preclinical Model
Nicholas W. Chavkin,
University of Virginia, USA
Hematopoietic Loss of the Y Chromosome Promotes Cardiac Fibrosis through Epigenetic Regulation of Autosomal Genes in Monocytes and Macrophages
Hematopoietic Loss of the Y Chromosome Promotes Cardiac Fibrosis through Epigenetic Regulation of Autosomal Genes in Monocytes and Macrophages
Thomas Martin,
University of Colorado Boulder, USA
Activation of FOXO1-dependent Autophagy Mediates Regression of Cardiac Hypertrophy
Activation of FOXO1-dependent Autophagy Mediates Regression of Cardiac Hypertrophy
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
2:30—4:30 PM
Workshop 2: Narrowing the Gap Between Discovery and Therapy in Pulmonary Hypertension
*
Stephen L. Archer,
Queen's University, Canada
*
Chanil Valasarajan,
Centre for Infection and Genomics of Lung, Justus Liebig University, Germany
Ke Yuan,
Boston Children's Hospital, USA
Deficiency of Smooth Muscle ADAR1 RNA Editing Exacerbates Vascular Remodeling and Pulmonary Hypertension
Deficiency of Smooth Muscle ADAR1 RNA Editing Exacerbates Vascular Remodeling and Pulmonary Hypertension
Sarasa Isobe,
Stanford University, USA
Loss of BMPR2 Links Unrepaired DNA Damage to Reduced FOXF1 and Pulmonary Arterial Hypertension
Loss of BMPR2 Links Unrepaired DNA Damage to Reduced FOXF1 and Pulmonary Arterial Hypertension
Tamanna Islam,
University of Texas at El Paso, USA
Bioengineering Models to Study Cell-Specific Durotaxis in Pulmonary Arterial Hypertension
Bioengineering Models to Study Cell-Specific Durotaxis in Pulmonary Arterial Hypertension
Emily J. Tsai,
Columbia University Vagelos College of Physicians & Surgeons, USA
In vivo Cardiac Myocyte-specific Knockdown of Wipi1 Prevents Decompensation of the Pressure-overloaded Right Ventricle
In vivo Cardiac Myocyte-specific Knockdown of Wipi1 Prevents Decompensation of the Pressure-overloaded Right Ventricle
Yingjie Chen,
University of Mississippi Medical Center, USA
Natural Killer Cells Regulate Heart Failure-induced Cardiopulmonary Inflammation, Pulmonary IFN-γ Production, and Pulmonary Remodeling
Natural Killer Cells Regulate Heart Failure-induced Cardiopulmonary Inflammation, Pulmonary IFN-γ Production, and Pulmonary Remodeling
Pontian Adogamhe,
Indiana University School of Medicine, USA
NAMPT Overexpression Decreases Sirt 3 Deacetylase Activity in Human Pulmonary Artery Endothelial Cells
NAMPT Overexpression Decreases Sirt 3 Deacetylase Activity in Human Pulmonary Artery Endothelial Cells
Olin Liang,
Brown University, USA
Targeting RUNX1 as a Novel Treatment Modality for Pulmonary Arterial Hypertension
Targeting RUNX1 as a Novel Treatment Modality for Pulmonary Arterial Hypertension
5:00—7:00 PM
Cell Responses to Myocardial Injury and Growth
*
Taben Hale,
University of Arizona, USA
*
Chi Fung Lee,
Oklahoma Medical Research Foundation, USA
Leslie A. Leinwand,
University of Colorado Boulder, USA
The Sarcomere is a Very Busy Place: From Bench to Bedside in Myosin Myopathies
The Sarcomere is a Very Busy Place: From Bench to Bedside in Myosin Myopathies
Kristine Deleon-Pennell,
Medical University of South Carolina, USA
T Cell Regulation of MI Remodeling
T Cell Regulation of MI Remodeling
Kathleen Woulfe,
University of Colorado Anschutz Medical Campus, USA
Short Talk: Age-specific Decreases in Sarcomeric Acetylation Modulates Myofilament Function in Skeletal and Cardiac Muscle
Short Talk: Age-specific Decreases in Sarcomeric Acetylation Modulates Myofilament Function in Skeletal and Cardiac Muscle
Ann Chiao,
Oklahoma Medical Research Foundation, USA
Short Talk: Aging Exacerbates Diastolic Dysfunction and Proteostatic Imbalance in Heart Failure with Preserved Ejection Fraction
Short Talk: Aging Exacerbates Diastolic Dysfunction and Proteostatic Imbalance in Heart Failure with Preserved Ejection Fraction
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
5:00—7:00 PM
Using Big Data to Understand Complex Disease
*
Micheala A. Aldred,
Indiana University, USA
Christopher Rhodes,
Imperial College London, UK
The Significance of Noncoding Variants in Pulmonary Hypertension
The Significance of Noncoding Variants in Pulmonary Hypertension
Wendy K. Chung,
Columbia University, USA
Penetrance of Mutations in Pediatric Pulmonary Hypertension
Penetrance of Mutations in Pediatric Pulmonary Hypertension
Jose Gomez-Arroyo,
University of Cincinnati, USA
Role of FOXF1 in the Pathobiology of Pulmonary Arterial Hypertension
Role of FOXF1 in the Pathobiology of Pulmonary Arterial Hypertension
Gabriel Maldonado-Velez,
Indiana University School of Medicine, USA
TBX4 Loss-of-function within the Embryonic Lung Mesenchyme Disrupts Lung Alveolar Development and Increases Susceptibility to Pulmonary Hypertension
TBX4 Loss-of-function within the Embryonic Lung Mesenchyme Disrupts Lung Alveolar Development and Increases Susceptibility to Pulmonary Hypertension
7:00—8:00 PM
On Own for Dinner
No registration fees are used to fund alcohol served at this function.
8:00—11:00 AM
Cardiometabolic Aspects of HF
*
Ann Chiao,
Oklahoma Medical Research Foundation, USA
*
Abraham L. Bayer,
Tufts Graduate School of Biomedical Sciences, USA
Rebecca Ritchie,
Monash Institute of Pharmaceutical Sciences, Australia
Diabetic Effects on Cardiac Remodeling
Diabetic Effects on Cardiac Remodeling
Susan E. Howlett,
Dalhousie University, Canada
The Many Effects of Aging and Frailty on the Heart
The Many Effects of Aging and Frailty on the Heart
Coffee Break
Helen E. Collins,
University of Louisville, USA
Mechanisms Contributing to Pregnancy-Induced Cardiac Growth
Mechanisms Contributing to Pregnancy-Induced Cardiac Growth
Chi Fung Lee,
Oklahoma Medical Research Foundation, USA
Short Talk: SARM1 Deficiency Prevents NAD Decline, Improve Mitochondrial and Cardiac Function in Cardiometabolic Disease
Short Talk: SARM1 Deficiency Prevents NAD Decline, Improve Mitochondrial and Cardiac Function in Cardiometabolic Disease
Kayla J. Rayford,
Meharry Medical College, USA
Short Talk: Trypanosoma Cruzi Alters Expression of piRNAs That Target Profibrotic and Inflammatory Molecules During Acute Infection of Primary Human Cardiac Fibroblasts
Short Talk: Trypanosoma Cruzi Alters Expression of piRNAs That Target Profibrotic and Inflammatory Molecules During Acute Infection of Primary Human Cardiac Fibroblasts
Kenneth Rockwood,
Dalhousie University, Canada
Short Talk: Assessing Frailty-related Mortality Risk in Older Adults Hospitalized with and without Congestive Heart Failure
Short Talk: Assessing Frailty-related Mortality Risk in Older Adults Hospitalized with and without Congestive Heart Failure
Adaysha Williams,
Medical College of Wisconsin, USA
Short Talk: High Inorganic Phosphate Treatment Reduces Rat Neonatal Cardiomyocyte Viability
Short Talk: High Inorganic Phosphate Treatment Reduces Rat Neonatal Cardiomyocyte Viability
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
8:00—11:00 AM
Using Biology to Guide Vascular Regeneration
*
James Klinger,
Alpert Medical School of Brown University, USA
*
YouYang Zhao,
Northwestern University-Lurie Children's Hospital of Chicago, USA
Vinicio de Jesus Perez,
Stanford University, USA
Restoring Normal Microvessels in Pulmonary Hypertension
Restoring Normal Microvessels in Pulmonary Hypertension
Rubin M. Tuder,
University of Colorado Hospital - Anschutz, USA
Disease Heterogeneity and the Challenges in Evaluating Therapies for a Complex Disease
Disease Heterogeneity and the Challenges in Evaluating Therapies for a Complex Disease
Coffee Break
David B. Frank,
Children's Hospital of Philadelphia, USA
Ontogeny and Cellular Heterogeneity in Pulmonary Vascular Development and Disease
Ontogeny and Cellular Heterogeneity in Pulmonary Vascular Development and Disease
Akiko Mammoto,
Medical College of Wisconsin, USA
Short Talk: Endothelial Senescence in Pulmonary Hypertension
Short Talk: Endothelial Senescence in Pulmonary Hypertension
3:00—4:30 PM
Career Roundtable (Joint)
Vinicio de Jesus Perez,
Stanford University, USA
Michael Dunn,
Regeneron Pharmaceuticals, USA
Chi Fung Lee,
Oklahoma Medical Research Foundation, USA
5:00—6:45 PM
Pharma Targets for Heart Failure
*
Helen E. Collins,
University of Louisville, USA
*
Yongneng Zhang,
University of Alberta, Canada
Zamaneh Kassiri,
University of Alberta, Canada
Metalloproteases Make It or Break It
Metalloproteases Make It or Break It
Rachel J. Roth Flach,
Pfizer Inc., USA
Metabolic Targets for Heart Failure
Metabolic Targets for Heart Failure
Michael Dunn,
Regeneron Pharmaceuticals, USA
Sustained Vasodilation in Preclinical Species and Humans by an Investigational Agonist Monoclonal Antibody to a Membrane-bound Guanylate Cyclase Receptor, Natriuretic Peptide Receptor 1
Sustained Vasodilation in Preclinical Species and Humans by an Investigational Agonist Monoclonal Antibody to a Membrane-bound Guanylate Cyclase Receptor, Natriuretic Peptide Receptor 1
Aina Hirofuji,
Asahikawa Medical University, Japan
Short Talk: Mycn Induces Cardiomyocyte Mitosis in Adult Mice
Short Talk: Mycn Induces Cardiomyocyte Mitosis in Adult Mice
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
5:00—6:45 PM
The Inflammatory Basis of Pulmonary Hypertension
*
Thomas Resta,
University of New Mexico HSC, USA
*
Andrew Bryant,
University of Florida College of Medicine, USA
Harry Karmouty-Quintana,
University of Texas Health Science Center, USA
RNA Translation and the Proteome of Pulmonary Hypertension
RNA Translation and the Proteome of Pulmonary Hypertension
Kurt R. Stenmark,
University of Colorado Denver, USA
The Interplay Between Fibroblasts and Monocytes in Pulmonary Hypertension
The Interplay Between Fibroblasts and Monocytes in Pulmonary Hypertension
Simon Bousseau,
National Jewish Health, USA
Short Talk: 17β-estradiol Regulates Angiogenesis and Right Ventricle Endothelial Cell Metabolism in Pulmonary Arterial Hypertension
Short Talk: 17β-estradiol Regulates Angiogenesis and Right Ventricle Endothelial Cell Metabolism in Pulmonary Arterial Hypertension
Benjamin Korman,
University of Rochester, USA
Short Talk: Single Cell RNA Sequencing of Mice with TNF-mediated Pulmonary Hypertension Demonstrates Marked Changes in Endothelial and Mesenchymal Cell Populations and Aberrant BMP Signaling
Short Talk: Single Cell RNA Sequencing of Mice with TNF-mediated Pulmonary Hypertension Demonstrates Marked Changes in Endothelial and Mesenchymal Cell Populations and Aberrant BMP Signaling
Following Session is for Pulmonary Hypertension: State of the Art and Therapeutic Opportunities (Z8)
7:00—8:00 PM
Social Hour with Lite Bites
No registration fees are used to fund alcohol served at this function.
*Session Chair †Invited, not yet responded.
Keystone Symposia thanks our Sponsors(s) for generously supporting this meeting:
We gratefully acknowledge the generous grant for this conference provided by:
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:
Click here to view more of these organizations
Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:
Click here to view more of these organizations
If your organization is interested in joining these entities in support of Keystone
Symposia, please contact: John Monson,
Director of Corporate Relations, Email: johnm@keystonesymposia.org, Phone:+1 970-262-2690 Click here for more information on Industry Support and Recognition Opportunities. If you are interested in becoming an advertising/marketing in-kind partner, please contact: Josh May, Director, Technology and Digital Media, Email: joshuam@keystonesymposia.org, Phone:+1 970-262-1179 |