Andrew GibbProfile page
Asst Professor Term
School of Medicine
- Asst Professor TermSchool of Medicine
- 502-852-9699 (Work)
- University of Louisville, Medicine, 580 S Preston, Louisville, KY, 40202, United States
SPONSORED PROJECTS
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.
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 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.
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.
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 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.
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.
SPONSORED PROJECTS
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