Gibb Lab

About 

The overall mission of the lab is to elucidate the causes and consequences of cardiac health and disease through the mechanistic interrogation of novel molecular and metabolic pathways. Our team utilizes a wide-range of techniques from discovery-based screens, multi-omic approaches, in vitro mechanistic studies, in vivo models of exercise and heart failure, and the generation of novel mutant animal models with a goal of discovering new therapies for the treatment and prevention of heart disease. 

View personal lab website

Team 

• Baladileep Annapureddy, Research Technician, baladileepreddy.annapureddy@louisville.edu
• Yu “Nancy” Tian, PhD Student, yu.tian@louisville.edu
• Christine Chen, M2 Distinction in Research Track, Christine.chen@louisville.edu
• Ryli Bulla, Junior Undergraduate Researcher (Biochemistry), Ryli.bulla@louisville.edu

Key Research Areas

Heart Failure 

Heart failure (HF) is characterized by a decrease in contractile function and maladaptive remodeling, including hypertrophy, inflammation, fibrosis, mitochondrial and metabolic dysfunction. Numerous ongoing projects in the lab are focused on identifying novel pathways which may be therapeutically targeted to treat heart disease. The lab uses murine models of HF including pressure overload, HFpEF, various mutant genetic models, and multi-omics approaches. 

Mitochondrial Energy Metabolism 

The heart is reliant on the continuous production of ATP to maintain function. During heart failure, a decrease in energy supply is a primary cause of poor function and ultimately negative cardiovascular outcomes. Therefore, it is imperative that we uncover novel means to improve the cardiac energy state through the targeting of metabolic energy producing pathways, with several projects in the lab ongoing in this area. 

Metabolite Transport 

Metabolite transport across plasma and organelle membranes is largely controlled by transporters and shuttle systems. We believe that disrupted transport may be the primary cause of metabolic dysfunction and have developed novel genetic approaches to test this hypothesis. We are also interested in whether metabolite transport across organelles is required to link metabolism to the epigenome. 

Fibroblast Activation & Reversal 

Fibrosis is the accumulation of excessive extracellular matrix proteins (ECM) and is mediated by the differentiation of fibroblast to myofibroblasts. This fibrosis results in tissue stiffening and poor cardiac function. Several ongoing project in the lab are focused on understanding the metabolic contributions to fibroblast differentiation and fibrosis as well as the identification of novel mechanisms mediating this process through molecular biology and NextGen Sequencing approaches.