Current projects in our lab focus on the biochemical mechanisms underlying how environmental stressors such as exposure to excessive alcohol, drugs, toxins, and even anxiety (perceived stress) impact cardiovascular development in utero. We are employing dynamic integrated systems biology approaches to better understand how particular forms of stress perturb metabolism leading to epigenetic modifications of DNA that, in turn, lead to critical changes in genome-wide RNA and protein expression patterns that ultimately result in structural and/or functional abnormalities that later manifest as congenital heart defects. By adopting these powerful new “big data” approaches, we aim to identify novel biomarkers and therapeutic targets that may be used, respectively, to successfully diagnose and treat stress-induced forms of congenital heart defects much earlier than presently possible, thereby creating the potential for improved clinical outcomes. A conceptual schematic using excessive ethanol as the stressor is depicted in the link provided:
Another project focuses on determining the cellular and molecular mechanisms responsible for adverse effects of stress on cardiovascular health later in life, with special emphasis on stress-induced cardiomyopathies (e.g., “Broken Heart Syndrome“) that primarily affect post-menopausal women. Please see the following publication link for a detailed description of our working “intrinsic cardiac adrenergic overload” hypothesis:
Baker CN, Katsandris R, Van C, and Ebert SN (2014) Adrenaline and Stress-Induced Cardiomyopathies: Three Competing Hypotheses for Mechanism(s) of Action.Chapter 4 (pp. 81-116) in book entitled, “Adrenaline: Production, Role in Disease and Stress, Effects on the Mind and Body”. Alfred Bennun, Editor. Nova Scientific Publishers, Inc. https://www.novapublishers.com/catalog/