A5074563344- Receptor Mechanisms and Signaling
- Cardiac Ischemia and Reperfusion
- Cardiovascular Function and Risk Factors
- Cardiac electrophysiology and arrhythmias
- Cardiac Fibrosis and Remodeling
- Adipose Tissue and Metabolism
- Hormonal Regulation and Hypertension
- Heart Failure Treatment and Management
- Heart Rate Variability and Autonomic Control
- Cardiac Imaging and Diagnostics
- Diet and metabolism studies
- Ion channel regulation and function
- Neuropeptides and Animal Physiology
- Eicosanoids and Hypertension Pharmacology
- Diabetes Treatment and Management
- Cardiovascular and exercise physiology
- Nitric Oxide and Endothelin Effects
- Cardiovascular Effects of Exercise
- Alzheimer's disease research and treatments
- Health Systems, Economic Evaluations, Quality of Life
- Cardiac Health and Mental Health
- Tissue Engineering and Regenerative Medicine
- Frailty in Older Adults
- Viral Infections and Immunology Research
- Lymphatic System and Diseases
Temple University
2013-2024
ASL Roma
2023-2024
Istituto Nazionale di Fisica Nucleare, Sezione di Napoli
2024
Istituti Clinici Scientifici Maugeri
2022
Center for Translational Molecular Medicine
2019
Fondazione Salvatore Maugeri
2012-2018
Imperial College London
2016-2018
University of Naples Federico II
2009-2017
SDN Istituto di Ricerca Diagnostica e Nucleare
2016
King's College London
2016
β-Arrestin (βarr)-1 and β-arrestin-2 (βarrs) are universal G-protein-coupled receptor adapter proteins that negatively regulate cardiac β-adrenergic (βAR) function via βAR desensitization downregulation. In addition, they mediate G-protein-independent signaling, which might be beneficial, for example, antiapoptotic, the heart. However, specific role(s) of each βarr isoform in dysfunction, molecular hallmark chronic heart failure (HF), remains unknown. Furthermore, adrenal βarr1 exacerbates...
Heart disease is the leading cause of hospitalization and death worldwide, severely affecting health care costs. Aging a significant risk factor for heart disease, senescent characterized by structural functional changes including diastolic systolic dysfunction as well left ventricular (LV) dyssynchrony. Speckle tracking–based strain echocardiography (STE) has been shown noninvasive, reproducible, highly sensitive methodology to evaluate LV function in both animal models humans. Herein, we...
Abstract Objectives To evaluate clinical outcomes in patients with diabetes, treated by cardiac resynchronization therapy a defibrillator (CRT-d), and glucagon-like peptide 1 receptor agonists (GLP-1 RA) addition to conventional hypoglycemic vs. CRTd under drugs. Background Patients diabetes experienced an amelioration of functional New York Association Heart class, reduction hospital admissions, mortality, percentage about 60%. However, 40% experience worse prognosis. Materials methods We...
Background Sepsis is the overwhelming host response to infection leading shock and multiple organ dysfunction. Cardiovascular complications greatly increase sepsis‐associated mortality. Although murine models are routinely used for preclinical studies, benefit of using genetically engineered mice in sepsis countered by discrepancies between human mouse pathophysiology. Therefore, recent guidelines have called standardization methods document We investigated course cardiac dysfunction...
Abstract Background β 1 - and 2 –adrenergic receptors (ARs) play distinct roles in the heart, e.g. AR is pro-contractile pro-apoptotic but anti-apoptotic only weakly pro-contractile. G protein coupled receptor kinase (GRK)-2 desensitizes opposes βAR signaling by phosphorylating inducing beta-arrestin (βarr) binding. We posited herein that GRK2 blockade might enhance of subtype heart. tested effects cardiac-targeted inhibition vivo exclusively on under normal conditions heart failure (HF)....
BACKGROUND AND PURPOSE Sympathetic nervous system (SNS) hyperactivity is characteristic of chronic heart failure (HF) and significantly worsens prognosis. The success β‐adrenoceptor antagonist (β‐blockers) therapy in HF primarily attributed to protection the from noxious effects augmented catecholamine levels. β‐Blockers have been shown reduce SNS HF, but underlying molecular mechanisms are not understood. GPCR kinase‐2 (GRK2)–α 2 adrenoceptor–catecholamine production axis up‐regulated...
Background: Caloric restriction (CR) has been described to have cardioprotective effects and improve functional outcomes in animal models humans. Chronic ischemic heart failure (HF) is associated with reduced cardiac sympathetic innervation, dysfunctional β-adrenergic receptor signaling, decreased inotropic reserve. We tested the of a long-term CR diet, started late after myocardial infarction on function, responsiveness rat model postischemic HF. Methods Results: Adult male rats were...
Abstract Aims Myocardial infarction (MI) is the most common cause of heart failure (HF) worldwide. G protein-coupled receptor kinase 5 (GRK5) upregulated in failing human myocardium and promotes maladaptive cardiac hypertrophy animal models. However, role GRK5 ischemic disease still unknown. In this study, we evaluated whether myocardial plays a critical post-MI mice included examination specific immune inflammatory responses. Methods results Cardiomyocyte-specific overexpressing transgenic...
To evaluate the prevalence of metabolic syndrome (MS) and its components in a population-based cohort, to analyse association between gender, environmental conditions, C-reactive protein (CRP), syndrome.Out 1877 subjects aged 45-64, who represented all patients six family physicians, representative sanitary districts Asti (north-western Italy), 88% accepted participate an interview on personal habits, several clinical laboratory measurements.The MS (National Cholesterol Education Program...
We investigated whether β(2) -adrenoceptor overexpression could promote angiogenesis and improve blood perfusion left ventricular (LV) remodeling of the failing heart.We explored angiogenic effects in a rat model post-myocardial infarction (MI) heart failure (HF). Cardiac adenoviral-mediated was obtained via direct intramyocardial injection 4-weeks post-MI. Adenovirus(Ad)-GFP saline injected rats served as controls. Furthermore, we extended our observation to -/- mice undergoing...
Background— Impaired angiogenesis in the post-myocardial infarction heart contributes to progression failure. The inhibition of vascular endothelial growth factor (VEGF) signaling has been shown be crucial for transition from compensatory hypertrophy cardiac Importantly, β-adrenergic receptor blocker therapy also improve myocardial perfusion by enhancing neoangiogenesis failing heart. Methods and Results— Eight weeks surgically induced infarction, failure rats were randomized receive...
Reperfusion as a therapeutic intervention for acute myocardial infarction-induced cardiac injury itself induces further cardiomyocyte death.β-arrestin (βarr)-biased β-adrenergic receptor (βAR) activation promotes survival signaling responses in vitro; thus, we hypothesize that this pathway can mitigate death at the time of reperfusion to better preserve function.However, lack efficacious βarr-biased orthosteric small molecules has prevented investigation into whether relays protection...
Sympathetic nervous system hyperactivity is associated with poor prognosis in patients heart failure (HF), yet routine assessment of sympathetic activation not recommended for clinical practice. Myocardial G protein-coupled receptor kinase-2 (GRK2) upregulated HF patients, causing dysfunctional β-adrenergic signaling. Importantly, myocardial GRK2 levels correlate found peripheral lymphocytes patients.The independent prognostic value blood measurements has never been investigated; thus, the...
Increased cardiac G protein-coupled receptor kinase-2 (GRK2) expression has a pivotal role at inducing heart failure (HF)-related β-adrenergic (βAR) dysfunction. Importantly, abnormalities of βAR signalling in the failing heart, including GRK2 overexpression, are mirrored circulating lymphocytes and correlate with HF severity. Exercise training been shown to exert several beneficial effects on normalization function protein levels. In present study, we evaluated whether lymphocyte levels...