Area of research
Physiology · Immunology
Research interest
Research interests include Telomeres, Telomerase, and Senescence, Neutrophil, Myeloperoxidase and Oxidative Mechanisms, Nitric Oxide and Endothelin Effects, and Circadian rhythm and melatonin.
Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies
MitoQ reduces senescence burden in doxorubicin-treated endothelial cells by reducing mitochondrial ROS and DNA damage
Endothelial-Specific Reduction in Arf6 Impairs Insulin-Stimulated Vasodilation and Skeletal Muscle Blood Flow Resulting in Systemic Insulin Resistance in Mice
Endothelial cell telomere dysfunction induces senescence and results in vascular and metabolic impairments
Glycocalyx-targeted therapy ameliorates age-related arterial dysfunction
Endothelial cell‐specific reduction in mTOR ameliorates age‐related arterial and metabolic dysfunction
Reduction of double-strand DNA break repair exacerbates vascular aging
Mechanisms and consequences of endothelial cell senescence
Aging results in DNA damage and telomere dysfunction that is greater in endothelial versus vascular smooth muscle cells and is exacerbated in atheroprone regions
Aging results in endothelial cell telomere uncapping that induces senescence and physiological dysfunction
T cells mediate cell non‐autonomous arterial ageing in mice
A Focused DNA-Encoded Chemical Library for the Discovery of Inhibitors of NAD<sup>+</sup>-Dependent Enzymes
Advanced age results in a diminished endothelial glycocalyx
The role of senescence, telomere dysfunction and shelterin in vascular aging
Induced Trf2 deletion leads to aging vascular phenotype in mice associated with arterial telomere uncapping, senescence signaling, and oxidative stress