Research Group

Condorelli Group

Immunology in Cardiovascular Pathologies Lab

Condorelli Group

Gianluigi Condorelli

Group Leader

Our lab aims at understanding the molecular mechanisms of cardiovascular diseases, particularly heart failure and the broad spectrum of molecular events that control myocardial function, with a multilevel, bench to bedside methodology.

The challenge

Heart failure is the clinical end-point of many cardiovascular diseases (CVDs), such as hypertension, myocardial infarction, cardiomyopathy and myocarditis. Despite the advancement in prevention and early diagnosis, these pathologies are the main cause of death and disabilities worldwide. By better understanding cellular and molecular mechanisms behind heart failure we could identify new therapeutic targets and dramatically improve the quality of life for millions of patients with CVDs.

Main research areas

Epigenetics of cardiovascular diseases

We want to understand how risk factors and tissue damage modify gene expression in cells of the cardiovascular system and how such dysregulated gene expression affect cells behavior in the context of heart failure and atherosclerosis.

Role of immune-inflammation in cardiovascular diseases

In collaboration with other research groups at Humanitas Research Hospital and Humanitas University, we study the role that innate and acquired immunity play in remodeling myocardial tissues and in atherosclerosis. Our final goal is to better understand the involvement of the immune system in cardiovascular diseases, leading the way towards new therapeutic approaches targeting inflammation in CVDs.

Innovative biomarkers of cardiovascular diseases

By studying the downstream molecules produced by gene expression reprogramming and immune-inflammation in CVDs, we aim at identifying new biomarkers with diagnostic and prognostic value for disease assessment.

Selected publications

Anselmo A
Eur Heart J
Myocardial hypoxic stress mediates functional cardiac extracellular vesicle release.
Martini E
Circulation
Single-Cell Sequencing of Mouse Heart Immune Infiltrate in Pressure Overload-Driven Heart Failure Reveals Extent of Immune Activation.
Salvarani N
Nat Commun
The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy.
Hall IF
Circ Res
Circ_Lrp6, a Circular RNA Enriched in Vascular Smooth Muscle Cells, Acts as a Sponge Regulating miRNA-145 Function.
Elia L
J Clin Invest
UHRF1 epigenetically orchestrates smooth muscle cell plasticity in arterial disease.
Papait R
Circulation
Histone Methyltransferase G9a Is Required for Cardiomyocyte Homeostasis and Hypertrophy.
Kallikourdis M
Nat Commun
T cell costimulation blockade blunts pressure overload-induced heart failure.
Lodola F
Cell Death Dis
Adeno-associated virus-mediated CASQ2 delivery rescues phenotypic alterations in a patient-specific model of recessive catecholaminergic polymorphic ventricular tachycardia.
Greco CM
Nat Commun
DNA hydroxymethylation controls cardiomyocyte gene expression in development and hypertrophy.
Greco CM
Nat Rev Cardiol
Epigenetic modifications and noncoding RNAs in cardiac hypertrophy and failure.
Climent M
Circ Res
TGFβ Triggers miR-143/145 Transfer From Smooth Muscle Cells to Endothelial Cells, Thereby Modulating Vessel Stabilization.
Roncarati R
J Am Coll Cardiol
Circulating miR-29a, among other up-regulated microRNAs, is the only biomarker for both hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy.
Papait R
Proc Natl Acad Sci U S A
Genome-wide analysis of histone marks identifying an epigenetic signature of promoters and enhancers underlying cardiac hypertrophy.
Zhang D
J Clin Invest
MTORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice.
Quintavalle M
J Cell Biol
MicroRNA control of podosome formation in vascular smooth muscle cells in vivo and in vitro.
Elia L
Circulation
Reciprocal regulation of microRNA-1 and insulin-like growth factor-1 signal transduction cascade in cardiac and skeletal muscle in physiological and pathological conditions.
Elia L
Cell Death Differ
The knockout of miR-143 and -145 alters smooth muscle cell maintenance and vascular homeostasis in mice: correlates with human disease.
Catalucci D
J Cell Biol
Akt regulates L-type Ca2+ channel activity by modulating Cavalpha1 protein stability.
Gallo P
Cardiovasc Res
Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure.
Carè A
Nat Med
MicroRNA-133 controls cardiac hypertrophy.
Condorelli G
Proc Natl Acad Sci U S A
Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice.

Group members

Condorelli Group
Gianluigi Condorelli

Group Leader

Condorelli Group
Javier Laura Francés

Postdoc fellow

Condorelli Group
Lorenzo Marcone

Bioinformatician

Condorelli Group
Michele Miragoli

Associate Professor, University of Parma

Condorelli Group
Elettra Musolino

Postdoc fellow

Condorelli Group
Christina Pagiatakis

Researcher, Insubria University

Condorelli Group
Laura Papa

Postdoc fellow

Condorelli Group
Roberto Papait

Associate Professor, Insubria University

Condorelli Group
Mauro Passaretti

PhD student

Condorelli Group
Marcello Rubino

Postdoc fellow

Condorelli Group
Nicolò Salvarani

CNR Senior researcher

Condorelli Group
Simone Serio

Bioinformatician