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Updated: Jan 8, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
Published on: June 14, 2020
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.
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.
Abstract:
Ageing populations present substantial healthcare challenges, with cardiovascular disease (CVD) remaining the predominant cause of morbidity and mortality globally. Cardiac ageing is characterised by progressive cellular and molecular changes, contributing to structural and functional decline and predisposition to CVD. Component proteins (nucleoporins) of the Nuclear Pore Complex (NPC) and the nuclear lamina are both crucial for nuclear integrity and chromatin organisation, and have appeared as key players in cellular homeostasis of post-mitotic cells. Age-related changes in NPC composition and turnover, particularly in non-dividing cells, compromise nucleocytoplasmic compartmentalisation and drive genomic instability, cell death, and senescence. Emerging evidence implicates aberrant NPC components in the core hallmarks of cardiac ageing and in distinct heart diseases. Additionally, the nuclear lamina's susceptibility to damage and its interactions with NPCs might exacerbate these effects. This review presents evidence linking NPC and nuclear lamina dysfunction to features of the ageing heart and suggests that age-related NPC alterations are potential drivers of cardiomyocyte and cardiac decline with age.
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