Ageing research has made significant progress over recent years, highlighting several hallmarks that are considered to contribute to the ageing process. Autophagy, a process of cellular recycling, is implicated in most of these ageing hallmarks. Autophagy declines with age and induction of autophagy has been shown to improve age-associated changes. This makes autophagy a promising therapeutic target. Unfortunately, there are only a handful of autophagy-inducing-drugs that have been shown to reverse ageing. These molecules have safety issue, which limit their use and make it essential to discover safer and more effective drugs. Recently, we found that a pathway controlling autophagy, called the TFEB pathway, is often dysregulated in age and crucial for the prevention of cellular ageing. Re-establishing TFEB expression in aged cells through therapeutic approaches can restore cellular functions and rejuvenate the cells. In our lab, we aim is to develop a drug enhancing the TFEB pathway to allieviate age-related molecular dysfunctions. This approach may hold the key to improve a broad range of age-associated morbidities and promote a 'healthier' aging.
Our overall aim is to identify the contribution of the age-related TFEB pathway to the development and progression of osteoarthritis and to use this knowledge to develop new treatments for OA.
Kennedy Professor of Translational Rheumatology and Director of Clinical Research