Richard Z. Lin,
An estimated 4.8 million Americans suffer from heart failure, and
more than 400,000 people die of this disease each year. Despite advances
in the treatment of heart failure, this illness is a progressive disease
with a high mortality rate. Clinical and animal studies suggest that
activation of G alpha q by G protein-coupled receptors plays a critical
role in the pathogenesis of heart failure. My laboratory investigates
the signaling pathways that control cell growth and survival, and how
alterations in these pathways lead to cardiac hypertrophy and heart
failure. Recently, our focus is on how Gq-coupled receptors and G alpha
q regulate the phosphatidylinositol (PI) 3-kinase signaling pathway.
We are also interested in how the lipid second messenger produced by
PI 3-kinase activates two downstream effectors, Akt and p70 S6 kinase.
These signaling molecules regulate important physiologic functions
such as apoptosis and protein synthesis. My laboratory employs biochemical
and molecular techniques in conjunction with physiological studies
in transgenic mouse models of heart failure. Understanding how these
signaling molecules are regulated during heart failure may lead to
the development of new treatments for this deadly disease.