心肌衰竭病程中細胞骨骼蛋白質結構變化之研究
Date Issued
2003-07-31
Date
2003-07-31
Author(s)
許榮彬
DOI
912314B002225
Abstract
Heart failure is defined as the pathologic state of impaired cardiac function rendering the
heart unable to maintain an output sufficient for the metabolic requirements of the body’s
tissues and organs. Heart failure refractory to medical treatment consumes an ever
increasing amount of health care resources. Heart failure is a major public health issue. It is a
major source of morbidity and mortality, is expensive to treat and is frequently treated
inappropriately.
Although progress has been made in our understanding of the basic pathophysiology of heart
failure, many mechanisms involved remain unclear. Applications of the techniques of
molecular and cell biology to the study of heart failure are providing new insights into the
mechanisms responsible for this important clinical problems. The basic mechanisms
involved include beta-adrenergic recepters, cytokines, nitric oxide, and apotosis. There is
some evidence indicating that cytoskeletal proteins like tubulin and desmin are also crucial for
development of pathologic processed leading to heart failure. Here, using an animal model
of LV pressure overload, we would like to investigate the in vivo structural changes of
cytoskeletal proteins during the evolution to heart failure. The two-dimensional gel
electrophoresis revealed that a small group of proteins are differentially expressed between
normal rats and those with one-month cardiac pressure overload. Thus far, we found that the
expression of two proteinase inhibitors was severely reduced. It should be intriguing to
explore whether enhanced proteinase activity might be involved in functional changes related
to heart failure. Nevertheless, these preliminary data showed that this model system should
be of great use in the studies about the cytoskeletal changes during the disease process.
Subjects
cytoskeleton
heart failure
post-translational modification
LC/MS/MS
SDGs
Publisher
臺北市：國立臺灣大學醫學院外科
Type
report
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