Member Spotlight

Rajasekaran Namakkal-Soorappan

u04319921Rajasekaran Namakkal-Soorappan, PhD:   - Assistant Professor, Dept. of Molecular and Cellular Pathology.  In July 2014, Dr. Namakkal-Soorappan came to UAB from the University of Utah Health Sciences Center, Salt Lake City, Utah, bringing with him an extensive history and knowledge in Cardiology.  He also worked with the Dept. of Exercise and Sport Science at the College of Health, at the University of Utah.  Dr. Namakkal-Soorappan is interested in the transcriptional mechanisms for reductive stress in the heart. Regulation of cytoprotective/antioxidant defense genes is crucial to maintain the redox homeostasis and steady/dynamic function of the myocardium. Nuclear erythroid 2-related factor 2 (Nrf2) is the master transcription factor that regulates numerous (over 100) genes, which code for key antioxidant enzymes. Turning ON or OFF the Nrf2 at will can exert desired effects in the intracellular redox milieu and/or redox signaling to regulate redox sensitive cardio-protective proteins.

Investigating the cause-and-effect relationships between the OXIDATIVE and REDUCTIVE conditions in the myocardium will allow us to understand the critical signals that result in physiological and/or pathological consequences leading to the development of cardiac disease.

To understand these relationships under acute and chronic settings, we have been using in vitro and in vivo models (cardiomyocyte cell cultures, transgenic/knockout mouse models) bearing oxidative or reductive stress. Subsequently, we determine whether or not the SHIFT in REDOX STATE in the context of cardiomyocyte could be a causal mechanism for important cardiac diseases including cardiac hypertrophy, cardiomyopathy, heart failure, myocardial infarction and cardiac arrest. The goal is to define the redox signals in cardiovascular pathophysiology and to develop potential therapeutic measures. Dr. Raj’s lab takes advantage of the leading-edge technology to develop appropriate in vitro and/or in vivo reductive stress models in the context of cardiomyocytes and the myocardium.

In the past (1995-2001), Raj has been engaged in the research to understand the biochemistry & metabolism of glutathione (GSH) - a major, ubiquitous non-protein thiol that exerts a great deal of antioxidant power to fight against free radicals generated under basal and/or stressed conditions in the cellular life. Chronic shifts in the redox homeostasis and antioxidant defense system has been linked to multiple biochemical disorders in experimental animal/cell models and in human as well. It has been a big question/picture in my mind that “whether maintaining the critical redox milieu can FIX all the problems in a living cell?” Addressing this particular question is my long-term scientific goal.

Raj`s laboratory is currently conducting research in these areas

·        Nrf2 dependent transcriptional mechanisms for reductive stress in cardiac hypertrophy, cardiomyopathy.

·        Developing REDUCTIVE STRESS cell and small animal (mouse) models.

·        Investigating fundamental mechanisms for transcriptional activation of antioxidant pathways under basal and
       stressed conditions.


·        Manipulation of Nrf2-antioxidant signaling in aging heart and skeletal muscle.

·        Nrf2 signaling based interventions (physical and drug) to improve clinical conditions associated
       with oxido-reductive stress in the heart.