Skip to main content
. Author manuscript; available in PMC: 2020 Jun 4.
Published in final edited form as: Annu Rev Biomed Eng. 2019 Mar 27;21:443–468. doi: 10.1146/annurev-bioeng-060418-052139

Figure 4.

Figure 4

Defective mechanotransduction as a bridge between laminopathy hypotheses. Structural defects (increased nuclear fragility that leads to breakage and cell death) and gene misregulation (altered gene activation and silencing) are the two primary hypothesized mechanisms responsible for the muscle-specific defects in many laminopathies. A third hypothesis—defective nuclear mechanotransduction—synthesizes both the structural disruption and gene misregulation hypotheses, as it can explain how downstream gene misregulation might be a product of nuclear weakness due to disruption of mechanotransduction mechanisms in and on the nucleus.