Dr. Aroumougame (“Thambi”) earned his Ph.D. from Banaras Hindu University in India and completed his postdoctoral training at Lawrence Berkeley National Laboratory in California. He joined UT Southwestern Medical Center in 2004, progressing from instructor to tenured Associate Professor in 2021. In December 2024, he joined the Sarver Heart Center at the University of Arizona, where he continues his research on DNA repair mechanisms, cardiovascular disease, premature aging, and radiation biology.
1. Our research focuses on understanding how genotoxic cancer therapies such as doxorubicin and radiotherapy contribute to long-term cardiovascular complications. These treatments generate reactive oxygen species (ROS) and DNA damage, yet the molecular mechanisms linking this damage to cardiac dysfunction remain poorly defined. We aim to elucidate how ROS signaling, DNA repair pathways, and cardiac remodeling processes drive therapy-induced hypertrophy and dysfunction. Ultimately, we seek to uncover the role of the DNA damage response (DDR) in cardiotoxicity, with the goal of developing strategies to protect the heart in cancer survivors.
2. In parallel, we are investigating the role of DNA repair defects in premature cardiac aging. Aging-related stressors, such as oxidative DNA damage and elevated ROS, promote cellular senescence and impair heart function. Our studies focus on WRN, a DNA helicase essential for repairing oxidative DNA damage. Mutations in WRN cause Werner syndrome, a progeroid disorder marked by premature aging and early-onset cardiovascular disease. WRN deficiency leads to persistent DNA damage and chronic DDR activation, accelerating cardiomyocyte senescence. We aim to define how WRN contributes to cardiac aging through both DNA repair and mitochondrial regulation.
3. We also explore the non-canonical roles of DNA repair proteins in immune signaling, particularly the cGAS-STING pathway. We investigate how factors from the non-homologous end-joining and homologous recombination pathways influence immune activation in response to DNA damage. Our goal is to harness these mechanisms to improve cancer immunotherapy and reduce normal tissue toxicity, including effects on the heart.
