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40. Laser, M., Willey, C.D., Jiang, W., Cooper, G. 4th, Menick, D.R., Zile, M.R., Kuppuswamy, D. Integrin activation and focal complex formation in cardiac hypertrophy. J Biol Chem. Nov 10; 275 (45): 35624-30 (2000).
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42. Müller, JG, Isomatsu, Y, Koushik, SV, O'Quinn, M, Xu, L, Kappler, CS, Hapke, E, Zile, MR, Conway, SJ, Menick, DR.Cardiac-specific expression and hypertrophic upregulation of Exon H1 of feline Na+-Ca2+ exchanger-promoter in transgenic mouse model. Circ. Res., 90:(In Press) 2002.
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My laboratory is involved in
the analysis of gene regulation in cardiac hypertrophy and failure.
Hypertrophy is one of the major compensatory mechanisms utilized
by the heart for sustaining chronic hemodynamic overloads and
consists of both changes in the expression of specific proteins
and a quantitative increase in total cardiac protein. The cardiac
hypertrophic response is characterized by an increase in cardiac
mass, contractile protein content and size of the individual
cardiocyte. This response provides an initial means for the heart
to compensate for hemodynamic insults. But, if the pathological
stimulus is prolonged or sufficiently severe, and the increase
in mass is insufficient to normalize ventricular wall stress,
decompensated hypertrophy or heart failure will occur. One of
the main goals in the study of hypertrophy is to elucidate the
components and pathways responsible for the development and maintenance
of adaptive responses and distinguish them, if possible, from
those responsible for the potentially pathological changes in
cardiocyte morphology and physiology that characterize the failing
heart. During hypertrophy there is a coordinate increase in the
overall level of transcription and translation and in particular
an increase in contractile protein content. This results in increased
myofilaments and improved contractile function. But along with
these compensatory changes, there is upregulation of genes which
are normally expressed in the embryonic heart. Importantly, the
upregulation or, in some cases, down-regulation of many of these
genes is associated with distinct pathophysiological phenotypes
in the hypertrophying and failing heart. Identifying the signaling
components, nuclear factors, and cis-elements mediating
the change in the expression of these genes could lead to the
identification of new therapeutic targets specific to the failing
heart.
Endowment
