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May 14, 2001The Journal of Cell BiologyOpen Access

Alterations at the Intercalated Disk Associated with the Absence of Muscle Lim Protein

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Key result

In mouse models of dilated cardiomyopathy, altered expression of cytoskeletal proteins leads to impaired myofibrillar function and altered intercalated disk composition, with N-RAP upregulation serving as a potential early marker.

Population

Mouse models for dilated cardiomyopathy: muscle LIM protein knockout mouse and tropomodulin-overexpressing…

Comparison

Genetic alteration vs Wild-type mice/cells

Design

Preclinical

Authors

EEElisabeth EhlerHeart Failure & TransplantRHRobert HorowitsNational Institutes of HealthCZChristian ZuppingerUniversity Hospital of Bern

Discussion

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Implication

No change to DCM care indicated from mouse data; leaves open N-RAP as human biomarker pending validation.

Structured PICO

P
Population
Mouse models for dilated cardiomyopathy (DCM): muscle LIM protein (MLP) knockout mouse and tropomodulin-overexpressing transgenic (TOT) mouse
I
Intervention
Genetic alteration (MLP knockout or tropomodulin overexpression)
C
Comparator
Wild-type mice/cells
O
Outcome
Cardiomyocyte cytoarchitecture and alterations at the intercalated diskssurrogate

In mouse models of dilated cardiomyopathy, altered cytoskeletal protein expression is associated with structural changes at the intercalated disks, and N-RAP upregulation may serve as an early marker for DCM development.

Cite This Study

Ehler et al. (2001) studied Dilated cardiomyopathy. Muscle LIM protein (MLP) knockout and tropomodulin overexpression vs. Wild-type cells was evaluated on Cardiomyocyte cytoarchitecture and intercalated disk composition. In mouse models of dilated cardiomyopathy, altered expression of cytoskeletal proteins leads to impaired myofibrillar function and altered intercalated disk composition, with N-RAP upregulation serving as a potential early marker.

synapsesocial.com/papers/6a0cc4d004164ea96334c2dfhttps://doi.org/10.1083/jcb.153.4.763
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Both hypertrophic and dilated cardiomyopathies are caused by mutation of the same gene, δ-sarcoglycan, in hamster: An animal model of disrupted dystrophin-associated glycoprotein complex1997 · 298 citations
  2. 2Altered patterns of cardiac intercellular junction distribution in hypertrophic cardiomyopathy.1996 · 177 citations
  3. 3Dissociated Spatial Patterning of Gap Junctions and Cell Adhesion Junctions During Postnatal Differentiation of Ventricular Myocardium1997 · 227 citations
  4. 4Extensive but Coordinated Reorganization of the Membrane Skeleton in Myofibers of Dystrophic (mdx) Mice1999 · 94 citations
  5. 5Impairment of the myocardial ultrastructure and changes of the cytoskeleton in dilated cardiomyopathy.1991 · 525 citations