Area of research
Pulmonary and Respiratory Medicine · Molecular Biology
Research interest
Research interests include Pulmonary Hypertension Research and Treatments, Mitochondrial Function and Pathology, Nitric Oxide and Endothelin Effects, and Cardiovascular Function and Risk Factors.
c-Myc promotes metabolic reprogramming in pulmonary hypertension via the stimulation of glutaminolysis and the reductive tricarboxylic acid cycle
Refracture-related bone transport of tibia: technical notes and preliminary clinical results in nineteen cases
SOX17 Deficiency Mediates Pulmonary Hypertension: At the Crossroads of Sex, Metabolism, and Genetics
Mitochondrial hyperfusion induces metabolic remodeling in lung endothelial cells by modifying the activities of electron transport chain complexes I and III
Nitration-mediated activation of the small GTPase RhoA stimulates cellular glycolysis through enhanced mitochondrial fission
The mitochondrial redistribution of eNOS is involved in lipopolysaccharide induced inflammasome activation during acute lung injury
Complex interplay between autophagy and oxidative stress in the development of pulmonary disease
Activation of the mechanosensitive Ca2+ channel TRPV4 induces endothelial barrier permeability via the disruption of mitochondrial bioenergetics
TGF-β1 attenuates mitochondrial bioenergetics in pulmonary arterial endothelial cells via the disruption of carnitine homeostasis
RAC1 nitration at Y32 IS involved in the endothelial barrier disruption associated with lipopolysaccharide-mediated acute lung injury
Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease
Ovine Models of Congenital Heart Disease and the Consequences of Hemodynamic Alterations for Pulmonary Artery Remodeling
ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS)
LPS-induced Acute Lung Injury Involves NF-κB–mediated Downregulation of SOX18
Asymmetric Dimethylarginine Stimulates Akt1 Phosphorylation via Heat Shock Protein 70–Facilitated Carboxyl-Terminal Modulator Protein Degradation in Pulmonary Arterial Endothelial Cells
Autophagy in neonatal hypoxia ischemic brain is associated with oxidative stress
Nitric oxide induces hypoxia ischemic injury in the neonatal brain via the disruption of neuronal iron metabolism
Endothelin-1 Induces a Glycolytic Switch in Pulmonary Arterial Endothelial Cells via the Mitochondrial Translocation of Endothelial Nitric Oxide Synthase