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Selected Publications


Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure.

Journal Article Circ Res · July 5, 2024 BACKGROUND: Heart failure (HF) is one of the leading causes of mortality worldwide. Extracellular vesicles, including small extracellular vesicles or exosomes, and their molecular cargo are known to modulate cell-to-cell communication during multiple cardi ... Full text Link to item Cite

Epigenetic mechanisms regulate sex differences in cardiac reparative functions of bone marrow progenitor cells.

Journal Article NPJ Regen Med · April 29, 2024 Historically, a lower incidence of cardiovascular diseases (CVD) and related deaths in women as compared with men of the same age has been attributed to female sex hormones, particularly estrogen and its receptors. Autologous bone marrow stem cell (BMSC) c ... Full text Link to item Cite

Cardiomyocyte-specific Adhesion G Protein-Coupled Receptor F5 (ADGRF5) participates in cardiac homeostasis

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Mitochondrial GRK2 Dependent Regulation of the Cellular and Transcriptional Composition after Myocardial Infarction

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Therapeutic Efficacy of a Novel Pharmacologic GRK2 Inhibitor in Mice Models of Heart Failure

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.

Journal Article J Am Heart Assoc · February 21, 2023 Background The mitochondrial mRNA-binding protein FASTKD1 (Fas-activated serine/threonine [FAST] kinase domain-containing protein 1) protects myocytes from oxidative stress in vitro. However, the role of FASTKD1 in the myocardium in vivo is unknown. Theref ... Full text Open Access Link to item Cite

Editorial: Cardiac regeneration

Journal Article Frontiers in Cardiovascular Medicine · January 1, 2023 Full text Open Access Cite

Enhanced NCLX-dependent mitochondrial Ca2+ efflux attenuates pathological remodeling in heart failure.

Journal Article J Mol Cell Cardiol · June 2022 Mitochondrial calcium (mCa2+) uptake couples changes in cardiomyocyte energetic demand to mitochondrial ATP production. However, excessive mCa2+ uptake triggers permeability transition and necrosis. Despite these established roles during acute stress, the ... Full text Open Access Link to item Cite

G protein-coupled receptor kinase 5 (GRK5) contributes to impaired cardiac function and immune cell recruitment in post-ischemic heart failure.

Journal Article Cardiovasc Res · January 7, 2022 AIMS: Myocardial infarction (MI) is the most common cause of heart failure (HF) worldwide. G protein-coupled receptor kinase 5 (GRK5) is upregulated in failing human myocardium and promotes maladaptive cardiac hypertrophy in animal models. However, the rol ... Full text Open Access Link to item Cite

Abstract 110: Human-Induced Pluripotent Stem Cell Derived Exosomal Protein Induce Cardiac Regeneration

Journal Article Circulation Research · September 3, 2021 Introduction: Cardiovascular diseases are the leading causes of death worldwide. After myocardial infarction (MI), there is a permanent loss of cardiomyocytes (CMs), and as the mammalian heart has lim ... Full text Cite

A peptide of the amino-terminus of GRK2 induces hypertrophy and yet elicits cardioprotection after pressure overload.

Journal Article J Mol Cell Cardiol · May 2021 G protein-coupled receptor (GPCR) kinase 2 (GRK2) expression and activity are elevated early on in response to several forms of cardiovascular stress and are a hallmark of heart failure. Interestingly, though, in addition to its well-characterized role in ... Full text Open Access Link to item Cite

Characterization of βARKct engineered cellular extracellular vesicles and model specific cardioprotection.

Journal Article Am J Physiol Heart Circ Physiol · April 1, 2021 Recent data supporting any benefit of stem cell therapy for ischemic heart disease have suggested paracrine-based mechanisms via extracellular vesicles (EVs) including exosomes. We have previously engineered cardiac-derived progenitor cells (CDCs) to expre ... Full text Open Access Link to item Cite

A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure.

Journal Article Sci Signal · March 30, 2021 Aberrant changes in gene expression underlie the pathogenesis and progression of pressure-overload heart failure, leading to maladaptive cardiac hypertrophy, ventricular remodeling, and contractile dysfunction. Signaling through the G protein Gq triggers m ... Full text Open Access Link to item Cite

MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis.

Journal Article Front Immunol · 2021 Cardiac fibrosis, a pathological condition due to excessive extracellular matrix (ECM) deposition in the myocardium, is associated with nearly all forms of heart disease. The processes and mechanisms that regulate cardiac fibrosis are not fully understood. ... Full text Open Access Link to item Cite

Genomic Binding Patterns of Forkhead Box Protein O1 Reveal Its Unique Role in Cardiac Hypertrophy.

Journal Article Circulation · September 2020 BACKGROUND: Cardiac hypertrophic growth is mediated by robust changes in gene expression and changes that underlie the increase in cardiomyocyte size. The former is regulated by RNA polymerase II (pol II) de novo recruitment or loss; the latter involves in ... Full text Open Access Link to item Cite

Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure.

Journal Article Circ Res · July 5, 2024 BACKGROUND: Heart failure (HF) is one of the leading causes of mortality worldwide. Extracellular vesicles, including small extracellular vesicles or exosomes, and their molecular cargo are known to modulate cell-to-cell communication during multiple cardi ... Full text Link to item Cite

Epigenetic mechanisms regulate sex differences in cardiac reparative functions of bone marrow progenitor cells.

Journal Article NPJ Regen Med · April 29, 2024 Historically, a lower incidence of cardiovascular diseases (CVD) and related deaths in women as compared with men of the same age has been attributed to female sex hormones, particularly estrogen and its receptors. Autologous bone marrow stem cell (BMSC) c ... Full text Link to item Cite

Cardiomyocyte-specific Adhesion G Protein-Coupled Receptor F5 (ADGRF5) participates in cardiac homeostasis

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Mitochondrial GRK2 Dependent Regulation of the Cellular and Transcriptional Composition after Myocardial Infarction

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Therapeutic Efficacy of a Novel Pharmacologic GRK2 Inhibitor in Mice Models of Heart Failure

Conference ASPET 2023 Annual Meeting Abstract - Cardiovascular Pharmacology · June 2023 Full text Cite

Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.

Journal Article J Am Heart Assoc · February 21, 2023 Background The mitochondrial mRNA-binding protein FASTKD1 (Fas-activated serine/threonine [FAST] kinase domain-containing protein 1) protects myocytes from oxidative stress in vitro. However, the role of FASTKD1 in the myocardium in vivo is unknown. Theref ... Full text Open Access Link to item Cite

Editorial: Cardiac regeneration

Journal Article Frontiers in Cardiovascular Medicine · January 1, 2023 Full text Open Access Cite

Enhanced NCLX-dependent mitochondrial Ca2+ efflux attenuates pathological remodeling in heart failure.

Journal Article J Mol Cell Cardiol · June 2022 Mitochondrial calcium (mCa2+) uptake couples changes in cardiomyocyte energetic demand to mitochondrial ATP production. However, excessive mCa2+ uptake triggers permeability transition and necrosis. Despite these established roles during acute stress, the ... Full text Open Access Link to item Cite

G protein-coupled receptor kinase 5 (GRK5) contributes to impaired cardiac function and immune cell recruitment in post-ischemic heart failure.

Journal Article Cardiovasc Res · January 7, 2022 AIMS: Myocardial infarction (MI) is the most common cause of heart failure (HF) worldwide. G protein-coupled receptor kinase 5 (GRK5) is upregulated in failing human myocardium and promotes maladaptive cardiac hypertrophy in animal models. However, the rol ... Full text Open Access Link to item Cite

Abstract 110: Human-Induced Pluripotent Stem Cell Derived Exosomal Protein Induce Cardiac Regeneration

Journal Article Circulation Research · September 3, 2021 Introduction: Cardiovascular diseases are the leading causes of death worldwide. After myocardial infarction (MI), there is a permanent loss of cardiomyocytes (CMs), and as the mammalian heart has lim ... Full text Cite

A peptide of the amino-terminus of GRK2 induces hypertrophy and yet elicits cardioprotection after pressure overload.

Journal Article J Mol Cell Cardiol · May 2021 G protein-coupled receptor (GPCR) kinase 2 (GRK2) expression and activity are elevated early on in response to several forms of cardiovascular stress and are a hallmark of heart failure. Interestingly, though, in addition to its well-characterized role in ... Full text Open Access Link to item Cite

Characterization of βARKct engineered cellular extracellular vesicles and model specific cardioprotection.

Journal Article Am J Physiol Heart Circ Physiol · April 1, 2021 Recent data supporting any benefit of stem cell therapy for ischemic heart disease have suggested paracrine-based mechanisms via extracellular vesicles (EVs) including exosomes. We have previously engineered cardiac-derived progenitor cells (CDCs) to expre ... Full text Open Access Link to item Cite

A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure.

Journal Article Sci Signal · March 30, 2021 Aberrant changes in gene expression underlie the pathogenesis and progression of pressure-overload heart failure, leading to maladaptive cardiac hypertrophy, ventricular remodeling, and contractile dysfunction. Signaling through the G protein Gq triggers m ... Full text Open Access Link to item Cite

MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis.

Journal Article Front Immunol · 2021 Cardiac fibrosis, a pathological condition due to excessive extracellular matrix (ECM) deposition in the myocardium, is associated with nearly all forms of heart disease. The processes and mechanisms that regulate cardiac fibrosis are not fully understood. ... Full text Open Access Link to item Cite

Genomic Binding Patterns of Forkhead Box Protein O1 Reveal Its Unique Role in Cardiac Hypertrophy.

Journal Article Circulation · September 2020 BACKGROUND: Cardiac hypertrophic growth is mediated by robust changes in gene expression and changes that underlie the increase in cardiomyocyte size. The former is regulated by RNA polymerase II (pol II) de novo recruitment or loss; the latter involves in ... Full text Open Access Link to item Cite

Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging.

Journal Article Am J Physiol Heart Circ Physiol · May 1, 2020 Nitric oxide (NO) and S-nitrosothiol (SNO) are considered cardio- and vasoprotective substances. We now understand that one mechanism in which NO/SNOs provide cardiovascular protection is through their direct inhibition of cardiac G protein-coupled recepto ... Full text Open Access Link to item Cite

Interleukin-10 Deficiency Alters Endothelial Progenitor Cell-Derived Exosome Reparative Effect on Myocardial Repair via Integrin-Linked Kinase Enrichment.

Journal Article Circ Res · January 31, 2020 Rationale: Systemic inflammation compromises the reparative properties of endothelial progenitor cell (EPC) and their exosomes on myocardial repair, although the underlying mechanism of loss of function of exosomes from inflamed EPCs is still obscure. Obje ... Full text Open Access Link to item Cite

Podoplanin neutralization improves cardiac remodeling and function after acute myocardial infarction.

Journal Article JCI Insight · July 9, 2019 Podoplanin, a small mucine-type transmembrane glycoprotein, has been recently shown to be expressed by lymphangiogenic, fibrogenic and mesenchymal progenitor cells in the acutely and chronically infarcted myocardium. Podoplanin binds to CLEC-2, a C-type le ... Full text Open Access Link to item Cite

Restricting mitochondrial GRK2 post-ischemia confers cardioprotection by reducing myocyte death and maintaining glucose oxidation.

Journal Article Sci Signal · December 11, 2018 Increased abundance of GRK2 [G protein-coupled receptor (GPCR) kinase 2] is associated with poor cardiac function in heart failure patients. In animal models, GRK2 contributes to the pathogenesis of heart failure after ischemia-reperfusion (IR) injury. In ... Full text Open Access Link to item Cite

Abstract 366: The Role of Mitochondrial Calcium Uniporter Complex in Cardiac Contractility and Function

Conference Circulation Research · August 3, 2018 Cardiac contractility is regulated by the intracellular Ca 2+ concentration fluxes which are maintained by multiple channels and transporters. Mitochondrial Calcium Uniporter (MCU) is the hi ... Full text Cite

Abstract 333: TNF Receptor Modulation of Progenitor Cells and Exosomes for Myocardial Repair

Conference Circulation Research · August 3, 2018 Our published studies, using TNFR1 and TNFR2 knockout (KO) mice have demonstrated that negative effects of TNF during ischemic tissue repair including enhanced apoptosis and inflammatory cytokines expression and signaling, is largely mediated by TN ... Full text Cite

Heterozygous deletion of AKT1 rescues cardiac contractility, but not hypertrophy, in a mouse model of Noonan Syndrome with Multiple Lentigines.

Journal Article J Mol Cell Cardiol · November 2017 Noonan Syndrome with Multiple Lentigines (NSML) is associated with congenital heart disease in form of pulmonary valve stenosis and hypertrophic cardiomyopathy (HCM). Genetically, NSML is primarily caused by mutations in the non-receptor protein tyrosine p ... Full text Open Access Link to item Cite

Abstract 82: Reduction of SHP2’s Phosphatase Activity Improves Cardiac Adaptation to Pressure and Volume Overload

Journal Article Circulation Research · July 22, 2016 Since the inability of the heart to adapt to pathological stress results in heart failure, supporting cardiac stress adaptation may improve clinical outcome. We hypothesized that the protein tyrosine phosphatase SHP2 controls adaptation by modulati ... Full text Cite

Decellularized amniotic membrane attenuates postinfarct left ventricular remodeling.

Journal Article J Surg Res · February 2016 BACKGROUND: Placenta and amnion have been suggested as sources of juvenile cells and tissues for use in surgical regenerative medicine. We previously determined the impact of amniotic epithelial cells induced to undergo epithelial-to-mesenchymal transition ... Full text Open Access Link to item Cite

Epithelial-to-Mesenchymal Transition Enhances the Cardioprotective Capacity of Human Amniotic Epithelial Cells.

Journal Article Cell Transplant · 2015 The amniotic epithelium consists of cells exhibiting mature epithelial cell characteristics, but also varying degrees of stemness. We tested the hypothesis that induction of epithelial-to-mesenchymal transition (EMT) in amniotic epithelial cells (AECs) der ... Full text Open Access Link to item Cite

Cardioprotection by placenta-derived stromal cells in a murine myocardial infarction model.

Journal Article J Surg Res · November 2013 BACKGROUND: Autologous cells for cell therapy of ischemic cardiomyopathy often display age- and disease-related functional impairment, whereas an allogenic immunotolerant cell product would allow off-the-shelf application of uncompromised donor cells. We i ... Full text Open Access Link to item Cite

Impact of heart failure on the behavior of human neonatal stem cells in vitro.

Journal Article J Transl Med · September 27, 2013 BACKGROUND: Clinical cardiac cell therapy using autologous somatic stem cells is restricted by age and disease-associated impairment of stem cell function. Juvenile cells possibly represent a more potent alternative, but the impact of patient-related varia ... Full text Open Access Link to item Cite