Abstract
In metazoans, a thin filamentous network referred to as the nuclear lamina plays an essential role in providing mechanical support to the nucleus. The major constituent of the nuclear lamina is type V intermediate filament proteins that are collectively referred to as lamins. A variety of diseases collectively termed laminopathies have been linked to mutations in genes encoding nuclear envelope proteins, in particular lamins, such as X-linked Emery Dreifus muscular dystrophy, dilated cardiomyopathy, Dunnigan type familial partial lipodystrophy and Hutchinson-Gilford progeria syndrome. Apart from laminopathies, genome-wide association studies have also been implicated nuclear lamins in the pathophysiology of type 2 diabetes mellitus, although little information in terms of the function of lamins in its pathogenesis. Our current review attempts to summarize risk factors of diabetes mellitus that could be attributable to lamin mutations and indirectly linked to lamin-associated factors identified in the last two decades.
Publisher
Innovation Publishing House Pte. Ltd.
Cited by
9 articles.
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