作者: Byambajav Buyandelger , Keat-Eng Ng , Snjezana Miocic , Izabela Piotrowska , Sylvia Gunkel
DOI: 10.1007/S00424-011-0961-2
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摘要: Muscle LIM protein (MLP, also known as cysteine rich 3 (CSRP3, CRP3)) is a muscle-specific-expressed LIM-only protein. It consists of 194 amino-acids and has been described initially factor involved in myogenesis (Arber et al. Cell 79:221–231, 1994). MLP soon became an important model for experimental cardiology when it was first demonstrated that deficiency leads to myocardial hypertrophy followed by dilated cardiomyopathy heart failure phenotype 88:393–403, 1997). At this time, the genetically altered animal develop devastating disease. Interestingly, found be down-regulated humans with (Zolk Circulation 101:2674–2677, 2000) mutations are able cause hypertrophic forms (Bos Mol Genet Metab 88:78–85, 2006; Geier 107:1390–1395, 2003; Hershberger Clin Transl Sci 1:21–26, 2008; Knoll 111:943–955, 2002; Circ Res 106:695–704, 2010; Mohapatra 80:207–215, 2003). Although considerable efforts have undertaken unravel underlying molecular mechanisms—how mutations, either organisms or human setting these diseases still unclear. In contrast, only precise knowledge mechanisms will allow development novel innovative therapeutic strategies combat otherwise lethal condition. The focus review on function cardiac mechanosensation we shall point possible future directions research.