Profile
Philip Eaton gained a BSc in Biochemistry from Queen Mary College, University of London in 1989 before completing his PhD studies at the University of Sussex. After post-doctoral work at the Institute of Psychiatry, he joined the Department of Cardiovascular Research at the Rayne Institute, St Thomas’ Hospital in 1995. He remained there for nearly 24 years within the School of Cardiovascular Medicine & Sciences at King’s College London. In 2019, he moved to the William Harvey Research Institute, Queen Mary University of London where he heads a group studying the molecular basis of redox sensing and signalling in the cardiovascular system.
Research
Group members
Dr. Rebecca Charles (BHF Intermediate Fellow): Dr. Hyunju Cho; Dr. Mariana Fernandez-Caggiano; Dr. Lorena Fernandez-Mosquera; Dr. Asvi Francois; Dr. Alisa Kamynina; Dr. Gundeep Kaur; Dr. Oleksandra Prysyazhna; Dr. Daniel Simoes De Jesus; Dr. Christopher Switzer
Summary
Oxidants, which can be produced in cells and tissues, have been causatively implicated in the pathogenesis of most major diseases. Whilst this paradigm is still prevalent, and oxidants may indeed play important roles in the disease etiology, it is now understood that they can also serve as regulatory entities that are important for the maintenance of homeostasis during health and disease. Oxidants can be sensed and transduced into a biological event via their reaction with select cysteine thiol side chains on some proteins. Such reactions can result in oxidative post-translational modifications of proteins that in some cases alter their function to enable adaptation and homeostasis. By identifying thiol-based redox sensor proteins susceptible to oxidant-dependent alterations in structure and function, it is hoped a better understanding of the biological significance of these modifications during cardiovascular health and disease can be gained. Indeed, in some cases we have developed new electrophilic drugs that modify precise redox regulated cysteines for therapeutic purposes to combat cardiovascular disease.
