The Blackwood Laboratory

Heart disease is the leading cause of mortality in the US and is often preceded by pathological cardiac hypertrophy due to chronic hypertension and sustained increases in cardiac afterload. While initially an adaptive response to maintain cardiac output and systemic blood supply, pathological cardiac hypertrophy eventually leads to a decompensated state of heart failure (HF). The initial adaptive aspect of hypertrophic growth requires increases in protein synthesis, which must be balanced by adequate protein folding, and degradation of misfolded, potentially toxic proteins. Without this balance, cardiac myocytes cannot maintain protein homeostasis, or proteostasis, which threatens functional cellular integrity and viability. The Blackwood laboratory is focused on elucidating novel mechanisms whereby proteostasis machinery in the heart protects against chronic systemic diseases, such as HF and global metabolic syndrome, translating these discoveries into novel therapeutics, and evaluating their efficacy in preclinical models of HF. Specifically, we have three directives guiding our research program: (1) Elucidate novel mechanisms for heart-directed inter-organ communication during metabolic syndrome (i.e. Axes of Cardiometabolic Health); (2) Determine mechanisms contributing to atrial dysfunction and remodeling during HF; and (3) Determine the contributions of resident cardiac fibroblasts to the pathogenesis of HF.