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Lamins and metabolism.

Chayki Charar1, Yosef Gruenbaum1

  • 1Department of Genetics, The Alexander Silberman Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem 91904, Israel chayki18@gmail.com gru@vms.huji.ac.il.

Clinical Science (London, England : 1979)
|December 16, 2016
PubMed
Summary
This summary is machine-generated.

Lamins, nuclear proteins, are linked to metabolic syndrome and diseases like familial partial lipodystrophy. Mutations disrupt cell metabolism pathways, affecting cell growth and fat regulation.

Keywords:
cell cycleinsulinlaminopathieslaminsmTORmetabolismnuclear organization

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Area of Science:

  • Cell Biology
  • Genetics
  • Metabolic Diseases

Background:

  • Lamins are nuclear intermediate filaments crucial for nuclear organization and cell division.
  • Mutations in lamin genes cause over 17 diseases (laminopathies), including muscle, neuronal, aging, and metabolic disorders.
  • Metabolic laminopathies are associated with metabolic syndrome and cellular dysfunctions.

Purpose of the Study:

  • To review the involvement of lamin genes in regulating cellular metabolism.
  • To discuss the link between lamin mutations and metabolic dysfunctions.
  • To explore therapeutic implications for metabolic laminopathies.

Main Methods:

  • Literature review of studies on lamins, laminopathies, and cellular metabolism.
  • Analysis of cellular and animal models of metabolic laminopathies.
  • Examination of the mechanistic target of rapamycin (mTOR) pathway and autophagy in affected cells.

Main Results:

  • Cells from metabolic laminopathy patients and models exhibit disrupted mTOR signaling, abnormal autophagy, and altered adipogenesis gene expression.
  • Mutations in lamins are linked to metabolic syndrome and specific lipodystrophy types.
  • Rapamycin treatment improved cellular fate in Hutchinson-Gilford progeria syndrome cells.

Conclusions:

  • Lamin gene dysfunction significantly impacts cellular metabolism.
  • Understanding lamin's role in metabolism offers insights into treating metabolic laminopathies.
  • Targeting pathways like mTOR may hold therapeutic potential.