Research team
Expertise
My research focuses on translational cardioimmunology and inflammation biology, aiming to identify novel therapeutic targets for cardiovascular and musculoskeletal diseases. I combine molecular pathology, advanced tissue-level phenotyping, and experimental models to understand disease mechanisms and translate these findings into innovative therapeutic strategies. My work includes the development and evaluation of immune-modulating approaches, including gene and cell therapies, within the broader field of regenerative medicine.
Mast cells in cardiovascular disease: Fibrosis, angiogenesis and atherogenesis
Abstract
Mast cells are increasingly recognized as critical regulators of cardiovascular physiology and pathology, with emerging evidence implicating them in fibrosis, angiogenesis, tissue regeneration, and atherosclerosis. Despite these advances, their integrative role across cardiovascular disease mechanisms remains insufficiently defined, limiting the development of targeted therapeutic strategies. This project aims to define how mast cell–mediated signaling networks drive cardiovascular remodeling and disease progression, with a focus on protease-dependent pathways (e.g., tryptase and chymase). We hypothesize that mast cells function as central orchestrators linking inflammation, vascular dysfunction, and tissue remodeling across cardiovascular contexts.Researcher(s)
- Promoter: Martin Leonardo
Research team(s)
Funding
- INTERNAT.
Project type(s)
- Research Project
Genetically Engineered MSCs for Neovascular Modulation in Atherosclerosis.
Abstract
This research focuses on the critical role of pathological angiogenesis, driven by vascular endothelial growth factor (VEGF) gradients from adventitial vasa vasorum, in atherosclerotic plaque progression and instability. Fragile intraplaque neovessels, characterized by discontinuous basement membranes and low junction density, result in intraplaque hemorrhage, rendering the plaque more vulnerable. The study proposes an ex vivo gene therapy using mesenchymal stem cells (MSCs) engineered to overexpress sFLT1, a soluble VEGF receptor, to inhibit abnormal angiogenesis, stabilize plaques, and reduce rupture risk. By blocking VEGF-driven angiogenesis with sFLT1, this approach prevents the formation of fragile intraplaque neovessels. MSCs, with their ability to home to injury sites and regenerative potential, serve as optimal carriers for gene therapy and provide a promising solution to treat atherosclerosis. We will use an appropriate model, the ApoE-/-Fbn1C1039G/+ mice, which exhibit advanced atherosclerotic plaques with intraplaque neovascularization, hemorrhage and plaque rupture. Given the global rise in cardiovascular disease and the need for novel therapeutic solutions, this research seeks to fill an important gap. Genetically engineered MSCs have transformative potential in preventing atherosclerotic plaque progression and rupture through their local action. Key innovations include: (1) targeted therapy, in which MSCs expressing sFLT1 precisely target diseased tissues; (2) local action, in which engineered MSCs act directly on damage sites, improving efficacy and minimizing systemic effects; (3) enhanced regenerative potential, through genetic modifications that improve tissue repair, fibrosis reduction and immune modulation; and (4) versatility, extending this approach to treat autoimmune diseases and cancer in addition to cardiovascular disease.Researcher(s)
- Promoter: De Meyer Guido
- Fellow: Martin Leonardo
Research team(s)
Funding
- BOF
Project type(s)
- Research Project