A role for long-lived nuclear envelope proteins in cardiac ageing

Mathew Shuen1, Regis R Lamberts1, Sean Coffey2

  • 1Department of Physiology, University of Otago, Dunedin, New Zealand; HeartOtago, University of Otago, Dunedin, New Zealand.

PubMed

Insights

Ageing hearts show dysfunction in nuclear pore complexes (NPCs) and nuclear lamina, impacting cell integrity. These changes contribute to cardiac ageing and increase susceptibility to cardiovascular disease.

Area of Science:

  • Gerontology
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Cardiovascular disease (CVD) is a leading cause of death globally, exacerbated by ageing populations.
  • Cardiac ageing involves cellular and molecular changes leading to functional decline and increased CVD risk.
  • Nuclear Pore Complexes (NPCs) and the nuclear lamina are vital for nuclear integrity and cellular homeostasis, especially in non-dividing cells.

Purpose of the Study:

  • To review the link between NPC and nuclear lamina dysfunction and cardiac ageing.
  • To explore how age-related changes in these structures contribute to heart decline.
  • To identify potential drivers of cardiomyocyte ageing and cardiac dysfunction.

Main Methods:

  • Literature review of studies on nuclear pore complexes, nuclear lamina, and cardiac ageing.
  • Analysis of evidence linking NPC and nuclear lamina alterations to cellular senescence and genomic instability.
  • Examination of the role of these structures in heart diseases associated with ageing.

Main Results:

  • Age-related changes in NPC composition and turnover compromise nucleocytoplasmic transport and genomic stability.
  • Dysfunctional NPCs and nuclear lamina are implicated in key features of cardiac ageing, including senescence and cell death.
  • Interactions between NPCs and the nuclear lamina may exacerbate age-related cardiac damage.

Conclusions:

  • Aberrant NPC components and nuclear lamina integrity are associated with cardiac ageing.
  • Age-related NPC alterations are suggested as potential drivers of cardiomyocyte and cardiac decline.
  • Targeting NPC and nuclear lamina pathways may offer therapeutic strategies for age-related heart conditions.

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