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Evidence for the Involvement of Type I Interferon in Pulmonary Arterial Hypertension
TLDR
Data indicate that type I IFN, via an action of IFNAR1, mediates PAH, a link between interferon (IFN) and pulmonary arterial hypertension (PAH). Expand
Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension
TLDR
It is demonstrated that rapamycin partially reversed the protein expression patterns of EndoMT, improved experimental PAH, and decreased the migration of human pulmonary artery endothelial cells, providing the proof of concept that Endo MT is druggable. Expand
Chemotherapy-induced pulmonary hypertension: role of alkylating agents.
TLDR
Clinical data and animal models demonstrated a plausible cause-effect relationship between alkylating agents and PVOD, and Clinicians should be aware of this uncommon, but severe, pulmonary vascular complication of alkyLating agents. Expand
Transient Receptor Potential Canonical Channels Are Required for in Vitro Endothelial Tube Formation*
TLDR
The data showed that TRPC channels are essential for in vitro tubulogenesis, both on endothelial cell line and on primary endothelial cells. Expand
Nebivolol for improving endothelial dysfunction, pulmonary vascular remodeling, and right heart function in pulmonary hypertension.
TLDR
Nebivolol could be a promising option for the management of PAH, improving endothelial dysfunction, pulmonary vascular remodeling, and right heart function, and until clinical studies are undertaken, routine use of β-blockers in PAH cannot be recommended. Expand
miR-223 reverses experimental pulmonary arterial hypertension.
TLDR
It is demonstrated that restoring the expression of miR-223 in lungs of rats with monocrotaline-induced PAH reversed established PAH and provided beneficial effects on vascular remodeling, pulmonary resistance, right ventricle hypertrophy, and survival. Expand
Maintaining Low Ca2+ Level in the Endoplasmic Reticulum Restores Abnormal Endogenous F508del‐CFTR Trafficking in Airway Epithelial Cells
TLDR
It is shown that a limited and a maintained ER calcium level is sufficient to inhibit the F508del–CFTR/calnexin interaction and to restore the cAMP‐dependent CFTR chloride transport, thus showing the correction of abnormal trafficking. Expand
Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension
TLDR
In vivo pharmacological activation of KCNK3 alleviated monocrotaline-induced PH, thus demonstrating that loss of KC NK3 is a key event in PAH pathogenesis and thus could be therapeutically targeted. Expand
Mitomycin-Induced Pulmonary Veno-Occlusive Disease: Evidence From Human Disease and Animal Models.
TLDR
MMC-induced PVOD in rats represents a unique model to test novel therapies in this devastating orphan disease and should be tested as a preventive therapy for MMC- induced PVod in humans and rats. Expand
Thapsigargin activates Ca²+ entry both by store-dependent, STIM1/Orai1-mediated, and store-independent, TRPC3/PLC/PKC-mediated pathways in human endothelial cells.
TLDR
Using pharmacological inhibitors or siRNA revealed that the PKCeta is required for Ca�+ entry, and pharmacological inhibition of the tyrosine kinase Src also reduced Ca²+ entry. Expand
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