A selection from the lab and from Sébastien's earlier work. The full, up-to-date list lives on Google Scholar.
Shows that losing the transcription factor PITX2C pushes atrial heart cells away from healthy energy metabolism and toward oxidative stress, pointing to a mechanism linking this well-known atrial fibrillation risk gene to heart-rhythm dysfunction.
Compares two spin-probe methods for detecting reactive oxygen species in zebrafish and lays out an optimized protocol for measuring oxidative stress in fish hearts and larvae — a tool for studying cardiovascular disease.
Introduces a live-imaging probe that tracks β-catenin in endothelial cells to reveal how vessel walls mature, showing that blood flow and cell junctions shape this process differently across the developing heart.
A review of how zebrafish have been used to model human heart-rhythm disorders such as long QT and Brugada syndrome, including the imaging and genetic tools available for studying arrhythmia in this model.
Shows that the transcription factor Nfatc1 drives formation of the cells that give heart valves their mechanical strength, tracked at single-cell resolution as the zebrafish valve forms.
Identifies the transcription factor HHEX as a master switch for VEGFC, FLT4 and PROX1, the genes that launch lymphatic vessel formation — a mechanism conserved from fish to mammals.
Shows that new blood vessels invade an injured zebrafish heart within hours of damage, and that blocking this early revascularization prevents the heart from regenerating at all.
Uses live imaging to track individual heart-valve cells as they arrive from the atrium and ventricle in two distinct layers, whose signaling depends on blood flow through the heart.
Shows that related growth factors can substitute for VegfA in building blood vessels, pointing to a route by which tumors resist anti-VEGF therapy, and engineers new molecules designed to block it.
Finds that removing the RNA-processing enzyme Dicer from vessel cells doesn't block basic blood vessel formation, but does let blood leak into the lymphatic system — pointing to a small-RNA-based control over how the two networks separate.