Area of research
Pulmonary and Respiratory Medicine · Physiology
Research interest
Research interests include Pulmonary hypertension, Medicine, Internal medicine, Biology, Mitochondrion, and Pulmonary artery.
Abstract 4366782: Pulmonary Hypertension Exhibits The Loss Of Capillaries, Leading To a Shift Toward Proliferative, Mesenchymal, and Hematopoietic Phenotypes
Mitochondria as a primary determinant of angiogenic modality in pulmonary arterial hypertension
Abstract 4146556: Stratifin is a critical target in Pulmonary Hypertension
Cytokine profiling in pulmonary arterial hypertension: the role of redox homeostasis and sex
Glucose-6-phosphate dehydrogenase deficiency contributes to metabolic abnormality and pulmonary hypertension
Endothelial eNAMPT drives EndMT and preclinical PH: rescue by an eNAMPT‐neutralizing mAb
Sex-specific stress response and HMGB1 release in pulmonary endothelial cells
Necrosis-Released HMGB1 (High Mobility Group Box 1) in the Progressive Pulmonary Arterial Hypertension Associated With Male Sex
Heme induces rapid endothelial barrier dysfunction via the MKK3/p38MAPK axis
Single Mutation in the <i>NFU1</i> Gene Metabolically Reprograms Pulmonary Artery Smooth Muscle Cells
Complex III Inhibition-Induced Pulmonary Hypertension Affects the Mitochondrial Proteomic Landscape
Inhibition of Anaplerosis Attenuated Vascular Proliferation in Pulmonary Arterial Hypertension
Focus on Early Events: Pathogenesis of Pulmonary Arterial Hypertension Development
Rats with a Human Mutation of NFU1 Develop Pulmonary Hypertension
Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension
Recurrent inhibition of mitochondrial complex III induces chronic pulmonary vasoconstriction and glycolytic switch in the rat lung
Metabolic Changes Precede the Development of Pulmonary Hypertension in the Monocrotaline Exposed Rat Lung
Redox regulation of epidermal growth factor receptor signaling during the development of pulmonary hypertension
Complex I dysfunction underlies the glycolytic switch in pulmonary hypertensive smooth muscle cells
The Sexual Dimorphism Associated with Pulmonary Hypertension Corresponds to a Fibrotic Phenotype
NADPH Oxidase 4 Is Expressed in Pulmonary Artery Adventitia and Contributes to Hypertensive Vascular Remodeling
Endothelin-1 Induces a Glycolytic Switch in Pulmonary Arterial Endothelial Cells via the Mitochondrial Translocation of Endothelial Nitric Oxide Synthase
Bosentan inhibits oxidative and nitrosative stress and rescues occlusive pulmonaryhypertension