Martin E. Young, DPhil

Young-martinAssociate Professor

Dept. of Medicine

Division of Cardiovascular Diseases

Contact Information:

Office Address:ZRB308
Phone: 205-934-2328
E-mail:This email address is being protected from spambots. You need JavaScript enabled to view it.
Websites: School of Medicine Faculty Profile

Education:

University of Oxford, United Kingdom

BA/MA, Biochemistry, 1995

University of Oxford, United Kingdom

D.Phil., Biochemistry, 1998

Post-Graduate Training:

Boston University

Postdoctoral Fellow, 1998-9

University of Texas-Houston
Postdoctoral Fellow, 1999-2001

Research Description:

Martin Young received his Bachelors, Masters, PhD degrees in Biochemistry from the University of Oxford.  Following postdoctoral training at Boston University and the University of Texas-Houston, Dr. Young held faculty appointments at the University of Texas-Houston and Baylor College of Medicine, before joining UAB.  Research in Dr. Young’s laboratory is focused on understanding how environmental factors, such as time-of-day and nutrition, influence cardiovascular health and disease.  Regarding time-of-day, the laboratory is actively identifying the role(s) of the circadian clock within the cardiomyocyte.  A broad objective of the laboratory has been to test the hypothesis that the circadian clock within the cardiomyocyte synchronizes responsiveness of the heart to diurnal variations in its environment.  Impairment of this molecular mechanism would therefore result in an inability of the heart to respond appropriately to the onset of such environmental influences (i.e., maladaptation).  The primary humoral factors currently under investigation are nutrients, such as glucose and fatty acids.  In the latter case, the heart exhibits dramatic time-of-day-dependent oscillations in its responsiveness to fatty acids.  Failure to respond adequately to increased fatty acid availability will result in accumulation of intramyocellular fatty acid derivatives.  The latter may play a significant role in the pathogenesis of myocardial contractile dysfunction observed during obesity and diabetes mellitus.  To address this line of reasoning, the laboratory has recently generated genetically modified mouse models in which the circadian clock is specifically impaired within cardiomyocytes.  These models have provided novel insights regarding the critical roles of the cardiomyocyte circadian clock.

Publications

DRC Membership Category:

Senior Scientist