James L Kirkland

 James L Kirkland

Mayo Clinic, USA

Find publications in PubMed

Longevity & Healthspan is an open access, peer-reviewed, interdisciplinary journal that publishes articles on all aspects of aging biology in the context of healthy aging or age-related disease. More specifically, the journal emphasizes advancing understanding of how age-related changes in structure and function become risk factors for or accompany age-related diseases or conditions, and the biology underlying healthy aging and longevity.

James Kirkland is Professor of Physiology and Medicine, Noaber Foundation Professor of Aging Research, and Director of the Robert and Arlene Kogod Center on Aging at the Mayo Clinic in Rochester, Minnesota. He received his MD from the University of Toronto, before undertaking a residency in internal medicine at Toronto General Hospital. He went on to obtain an MSc in Geriatric Medicine from the University of Manchester, UK, before returning to the University of Toronto to study for a PhD at the Institute of Medical Science.

Research in his laboratory focuses on the impact of age and fat depot origin on the function of adipose tissue. Studying preadipocytes, his group has found that their capacity to differentiate into fat cells declines in aging individuals, correlating with a downregulation of adipogenic transcription factors and increased preadipocyte senescence. His group has also found that human and rat preadipocytes from different fat depots possess distinct morphologies, replication potentials, developmental regulator profiles, and susceptibilities to senescence. They are also examining the molecular mechanisms underpinning these observations, with the aim of unveiling novel targeted strategies to treat the age-related metabolic disease.

The goal of his group’s current research is to understand the mechanisms underlying changes in adipogenic transcription factors, stress response system activity, and cellular senescence with aging, in particular how these changes are affected by manipulation of telomere expression, reactive oxygen species generation, pharmacological interventions, and metabolic signaling.