Unraveling Nesprin's Role in Dilated Cardiomyopathy
Nesprins (nuclear envelope spectrin repeat proteins) are crucial components of the LINC (Linker of Nucleoskeleton and Cytoskeleton) complex, which helps connect the nuclear envelope to the cytoskeleton, facilitating nuclear positioning, mechanotransduction, and signal transduction. Mutations or dysfunction in nesprin proteins, particularly Nesprin-1 and Nesprin-2, have been implicated in various cardiac diseases, including dilated cardiomyopathy (DCM).
Dilated cardiomyopathy is characterized by the enlargement and impaired contraction of the heart's ventricles, leading to heart failure. Nesprins play a critical role in maintaining the structural integrity of the heart's muscle cells. Mutations in nesprin genes may lead to disrupted mechanical stability of the nucleus and altered gene expression, resulting in weakened heart muscle fibers and contributing to the development of DCM.
Studies have shown that nesprin mutations can impair mechanotransduction pathways, leading to defective muscle function and remodeling, which are hallmarks of dilated cardiomyopathy. Understanding the specific molecular mechanisms by which nesprins influence heart muscle function and contribute to DCM can provide potential therapeutic targets for treating the disease.
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#DilatedCardiomyopathy
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#MolecularCardiology
#LINCComplex
#HeartHealth
#Mechanotransduction
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