Sébastien Bonnet

This study uses multi-omic profiling to identify renal mechanisms in PAH, revealing structural and metabolic changes and potential therapeutic targets.

This study shows that 17β-estradiol promotes right ventricle angiogenesis through estrogen receptor α and apelin signaling in pulmonary hypertension.

This study identifies hypusine signaling as a driver of vascular smooth muscle cell proliferation in restenosis and shows that inhibiting DHPS reduces neointimal hyperplasia in preclinical models and human tissue.

PeptiDIA enhances peptide identification in fast-gradient DIA data using machine learning, improving identification depth by 25-34% in human and murine datasets.

This study identifies metabolic and inflammatory changes in the liver of PAH patients using single nucleus RNA sequencing, revealing distinct cellular phenotypes and signaling pathways.

The paper investigates the role of cardiac myofibroblasts and UCP2 SNPs in right ventricular failure in pulmonary arterial hypertension, finding increased cMFB and reduced UCP2 associated with decompensation.

This study identifies a sexually dimorphic NLRP3 signaling pathway in right ventricular failure, showing estrogen receptor α mediates protection against NLRP3-induced contractile dysfunction in cardiomyocytes.

This study develops preclinical models of Group-2 pulmonary hypertension and shows that levosimendan improves cardiac function and reduces pulmonary vascular inflammation and remodeling.

This study shows that inhibiting Epac1 with AM-001 reduces fibroblast proliferation and profibrotic markers, protecting against pulmonary fibrosis in mouse models and human lung slices.

The paper identifies FABP4/5 as key regulators of endothelial glycolysis and arterial programming in pulmonary hypertension using single-cell and spatial transcriptomics.

The study identifies integrin α5β1 as a key driver of pulmonary vascular remodeling in PAH and shows its inhibition improves hemodynamics and RV function in preclinical models.

This study identifies ATP-citrate lyase as a driver of vascular remodeling in pulmonary hypertension and coronary artery disease, showing its inhibition can reverse pathological changes.

This study shows that targeting Snai1 in the right ventricle rescues pulmonary hypertension-induced failure by reducing EndMT, fibrosis, and FMT through a LOXL2-dependent mechanism.

The paper uses scRNA-seq to identify disease-specific endothelial and stromal cell populations involved in arterial remodeling in PAH, highlighting TM4SF1 as a potential therapeutic target.

This paper classifies PAH-related genes based on evidence strength using a semi-quantitative scoring system, identifying twelve genes with definitive evidence and recommending their inclusion in genetic testing panels.