At the University of Edinburgh, Mark Nixon, PhD, recently became a principal investigator as he seeks to unlock the mysteries of developing cardiovascular disease and its link to obesity and type 2 diabetes. He reminisces about his first experiments as a child as well as why he’s staying in academia.
Mark Nixon, PhD, recently entered his seventh postdoctoral year and has embarked on a new role as a principal investigator at the Centre for Cardiovascular Science at the University of Edinburgh. With his new five-year Intermediate Research Fellowship funded by the British Heart Foundation, Nixon is focusing on tissue-specific mechanisms that regulate glucocorticoid delivery to, and export from, inflamed tissues.
Endocrine News spoke with Nixon to learn more about how the young researcher’s interests guided him to where he is today.
Endocrine News: Do you remember what first sparked your love of science?
Nixon: Like many other scientists, my interest in science started with a huge curiosity for nature and a love of mammalian physiology. I still remember sitting at my kitchen table as a child looking at insects under the microscope from my first “science kit,” and then being ordered to clean up the mess before dinner! The discovery of this microscopic world, one that determines how, for example, the cells in our bodies respond to different situations, has fascinated me ever since and it’s why I love what I do.
While my research interests were initially piqued at undergraduate level by the role of immune cell signalling in atherosclerosis, my focus shifted during my PhD towards investigating the underlying mechanisms of two of the biggest risk factors for developing cardiovascular disease — obesity and type 2 diabetes.
EN: Have your research interests always been in endocrinology and obesity-related issues?
Nixon: It’s inescapable that cardiovascular disease remains the largest single cause of death, not only here in the UK, but globally. While my research interests were initially piqued at undergraduate level by the role of immune cell signalling in atherosclerosis, my focus shifted during my PhD towards investigating the underlying mechanisms of two of the biggest risk factors for developing cardiovascular disease — obesity and type 2 diabetes. At the time, the field of adipose biology was really taking off, with adipose tissue being redefined as an endocrine organ. In an age when we are less likely to undergo nutritional stress, i.e., starvation, I became fascinated with how the body evolved its response to glucocorticoids, and how such mechanisms may have become maladaptive over time.
EN: How did your relationship with The British Heart Foundation begin?
Nixon: The British Heart Foundation has been at the core of cardiovascular research at the University of Edinburgh for a number of years. Our Centre for Cardiovascular Science was established as one of the founding four (now six) BHF Centres of Research Excellence in the UK, tasked with investing in promising young scientists and world-class facilities. So, my relationship with the BHF has been fostered over my years working here as a postdoctoral researcher. More recently, that relationship has grown as I sought independent funding to establish my own research group, and this past year I was awarded an Intermediate Research Fellowship to determine how delivery of glucocorticoids to adipose tissue is determined by inflammatory regulation of its circulating binding globulin CBG (corticosteroid binding globulin).
EN: Can you share more about current work?
Nixon: While we know that glucocorticoid excess in adipose tissue drives increased cardiovascular disease risk, therapeutic manipulations of already established regulators of intracellular glucocorticoid action have not progressed beyond phase II trials due to insufficient efficacy on metabolic outcomes. My post-doctoral studies began exploring additional mechanisms to control adipose tissue glucocorticoid levels. From this work I identified transmembrane export via ABCC1 as a mechanism limiting the action of corticosterone, but not cortisol, in adipocytes (see Nixon M, et al. in Science Translational Medicine, August 2016). More recently, we have exciting preliminary data that inflammatory-mediated cleavage of the circulating glucocorticoid binding protein CBG (corticosteroid binding globulin) may enhance delivery of glucocorticoids to obese adipose tissue. We are using a combination of murine and human in vivo, ex vivo, and in vitro models to study this mechanism.
My hope is that by the end of this fellowship, my group will have expanded to encompass several new strands of research — finding researchers from different backgrounds with new ideas who are smarter than me is something I’m really looking forward to, and something I know is crucial to the sustained success of a group.
EN: What are your plans after your fellowship ends? Will you stay in academia?
Nixon: At the moment, my focus is very much on getting my lab up and running and starting to piece together the best strategy for delivering translational research. My hope is that by the end of this fellowship, my group will have expanded to encompass several new strands of research — finding researchers from different backgrounds with new ideas who are smarter than me is something I’m really looking forward to, and something I know is crucial to the sustained success of a group. As for staying in academia, I certainly aim to be here for many more years, but I’m aware that despite its rewards, it can be a difficult and challenging career path. Thankfully, I am fortunate to be surrounded by a number of wonderful and supportive colleagues and mentors.
—Fauntleroy Shaw is a freelance writer based in Carmel, Ind. She is a regular contributor to Endocrine News.