Steeve Provencher

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.

This study shows that impaired BCAA metabolism promotes ferroptosis, leading to pulmonary arterial hypertension and associated liver disease, and that targeting BCAA metabolism can alleviate these effects.

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

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 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.