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Nuclear remodeling drives age-related cardiac dysfunction

We found that aging is accompanied by a reduction in cardiomyocyte nuclear size and increased stiffness, dependent on loss of A-type lamins. Mechanistically, age-dependent nuclear remodeling represses expression of cardiogenic transcription factors that are required for heart contractility. Preserving lamin or transcription factors delays cardiac decline.

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Fig. 1: Age-dependent cardiomyocyte nuclear remodeling by Lamin C loss.


  1. Chiao, Y. A. & Rabinovitch, P. S. The aging heart. Cold Spring Harb. Perspect. Med. 5, 1–15 (2015). A review article that describes the mechanisms of age-dependent heart dysfunction.

    Article  CAS  Google Scholar 

  2. Kirby, T. J. & Lammerding, J. Emerging views of the nucleus as a cellular mechanosensor. Nat. Cell Biol. 20, 373–381 (2018). A review article that describes mechanotransduction and the role of the nucleus.

    Article  CAS  Google Scholar 

  3. Ho, R. & Hegele, R. A. Complex effects of laminopathy mutations on nuclear structure and function. Clinical Genetics 95, 199–209 (2019). A review article that describes the mechanisms of age dependent heart dysfunction.

    Article  CAS  Google Scholar 

  4. Zhao, H. et al. Destabilizing heterochromatin by APOE mediates senescence. Nat. Aging 2, 303–316 (2022). A research article that presents a mechanism of age-related lamin A/C loss by APOE-dependent autophagy.

    Article  Google Scholar 

  5. Scaffidi, P. & Misteli, T. Lamin A-dependent nuclear defects in human aging. Science 312, 1059–1063 (2006). A research article that demonstrates conserved nuclear remodeling in progeria syndrome and aged donor fibroblasts.

    Article  CAS  Google Scholar 

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This is a summary of: Kirkland, N. J. et al. Age-dependent Lamin changes induce cardiac dysfunction via dysregulation of cardiac transcriptional programs. Nat. Aging, (2022).

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Nuclear remodeling drives age-related cardiac dysfunction. Nat Aging 3, 15–16 (2023).

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