Research Group
Elia Group
Vascular Epigenetics Lab
Our group aims at understanding the involvement of epigenetics in the development of vascular diseases, by studying new molecular pathways that regulate vascular smooth muscle and endothelial cell biology and in which DNA methylation, histone modifications, and non-coding RNAs expression play a major role.
The challenge
All vascular pathologies belong to the vast category of cardiovascular diseases (CVDs), that are responsible for 31% of global deaths and constitute and are the main cause of death and disability worldwide. Regardless of the specific vascular pathology, altered genes expression – and thus epigenetic mechanisms – are central to disease initiation and progression. Although current knowledge regarding epigenetic mechanisms in CVD development is still limited, the dramatic improvement in DNA and RNA sequencing capacity has accelerated our ability to detail the complex epigenetic landscapes of multiple pathological contexts, paving the way to the translation of the first discoveries to the clinic.
Main research areas
Non-coding RNAs in vascular cell biology
Early work conducted at the University of California, San Diego, was the first to demonstrate that small non-coding RNAs (namely, miR-143 and miR-145) are necessary for maintaining the contractile phenotype of vascular smooth cells (VSMCs) and, thus, regulate vascular tone and functionality in pathological conditions. This finding was fundamental in seeding the new concept of the centrality of these cells in cardiovascular disease development and for the recent discoveries that miRNAs also act as communication molecules, modulating vascular endothelial cell and macrophage functionalities by migrating directly from one cell type to another.
Epigenetics and vascular diseases
We are interested in how pathological stimuli alter gene expression through chromatin remodeling and how such mechanisms are involved in vascular disease development. We recently identified two proteins that play a key role in vascular smooth muscle cells biology leveraging on epigenetics mechanisms: a DNA methylation reader that plays a fundamental role in the regulation of VSMCs plasticity both in physiology and in vascular disease, and a gene transcription regulator that appears to play a key role in vascular inflammation.
Selected publications
Vascular malformation rupture in a patient affected by Costello syndrome.
The epigenetic enzyme DOT1L orchestrates vascular smooth muscle cell-monocyte crosstalk and protects against atherosclerosis via the NF-κB pathway.
Aggravation of pulmonary fibrosis after knocking down the aryl hydrocarbon receptor in the insulin-like growth factor 1 receptor pathway.
rs41291957 controls miR-143 and miR-145 expression and impacts coronary artery disease risk.
miR-9-5p is involved in the rescue of stress-dependent dendritic shortening of hippocampal pyramidal neurons induced by acute antidepressant treatment with ketamine.
miR-128-3p Is a Novel Regulator of Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Diseases.
Epigenetics and vascular diseases.
Circ_Lrp6, a Circular RNA Enriched in Vascular Smooth Muscle Cells, Acts as a Sponge Regulating miRNA-145 Function.
The involvement of epigenetics in vascular disease development.
UHRF1 epigenetically orchestrates smooth muscle cell plasticity in arterial disease.
MicroRNA-26a/cyclin-dependent kinase 5 axis controls proliferation, apoptosis and in vivo tumor growth of diffuse large B-cell lymphoma cell lines.
Ferritin, cellular iron storage and regulation.
Epigenetics and Vascular Diseases: Influence of Non-coding RNAs and Their Clinical Implications.
T cell costimulation blockade blunts pressure overload-induced heart failure.
Circular RNAs and heart failure: new players for an old disease.
MicroRNAs and pulmonary hypertension: a tight link.
TGFβ Triggers miR-143/145 Transfer From Smooth Muscle Cells to Endothelial Cells, Thereby Modulating Vessel Stabilization.
MiR-143/145 deficiency attenuates the progression of atherosclerosis in Ldlr-/-mice.
MicroRNA-133 modulates the β1-adrenergic receptor transduction cascade.
Group members
