Shakil Khan, Ph.D.Research Professional Department of Medicine
My research focusses on studying the mechanisms by which Intermittent Hypoxia inhibits Mitochondrial complex I activity. The study reveals three novel findings: (i) IH-evoked mitochondrial complex I inhibition requires Reactive Oxygen Species generation by NADPH Oxidase 2 and Ca2+-dependent S-glutathionylation of complex I subunits, (ii) inhibition of complex I increases mitochondrial ROS, and (iii) mitochondrial ROS contributes to sustained but not transient elevations in blood pressure in IH-treated rats.
- H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea
- Epigenetic regulation of redox state mediates persistent cardiorespiratory abnormalities after long-term intermittent hypoxia
- HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidase
- Impairment of pancreatic β-cell function by chronic intermittent hypoxia
- Mutual antagonism between hypoxia-inducible factors 1α and 2α regulates oxygen sensing and cardio-respiratory homeostasis
- Angiotensin II evokes sensory long-term facilitation of the carotid body via NADPH oxidase
For a complete list of publications click here:
- Ph.D., Aligarh Muslim University, Aligarh, India
Updated 4 years ago.