Nuclear mechanosignaling in striated muscle diseases

Frontiers in Physiology

Physiology

Bo Zhang¹  Joseph D. Powers¹  Andrew D. McCulloch²  Neil C. Chi³ 

[1] Department of Bioengineering, University of California San Diego, La Jolla, CA, United States;Department of Bioengineering, University of California San Diego, La Jolla, CA, United States;Institute for Engineering in Medicine, University of California San Diego, La Jolla, CA, United States;Department of Bioengineering, University of California San Diego, La Jolla, CA, United States;Institute for Engineering in Medicine, University of California San Diego, La Jolla, CA, United States;Department of Medicine, Division of Cardiovascular Medicine, University of California San Diego, La Jolla, CA, United States;Institute of Genomic Medicine, University of California San Diego, La Jolla, CA, United States;

关键词: mechanosignaling;    nucleus;    myocytes;    nucleoskeleton;    nuclear morphology;    LINC complex;    cardiomyopathy;    laminopathy;   

DOI  :  10.3389/fphys.2023.1126111

 received in 2022-12-17, accepted in 2023-02-22,  发布年份 2023

来源: Frontiers

【 摘 要 】

Mechanosignaling describes processes by which biomechanical stimuli are transduced into cellular responses. External biophysical forces can be transmitted via structural protein networks that span from the cellular membrane to the cytoskeleton and the nucleus, where they can regulate gene expression through a series of biomechanical and/or biochemical mechanosensitive mechanisms, including chromatin remodeling, translocation of transcriptional regulators, and epigenetic factors. Striated muscle cells, including cardiac and skeletal muscle myocytes, utilize these nuclear mechanosignaling mechanisms to respond to changes in their intracellular and extracellular mechanical environment and mediate gene expression and cell remodeling. In this brief review, we highlight and discuss recent experimental work focused on the pathway of biomechanical stimulus propagation at the nucleus-cytoskeleton interface of striated muscles, and the mechanisms by which these pathways regulate gene regulation, muscle structure, and function. Furthermore, we discuss nuclear protein mutations that affect mechanosignaling function in human and animal models of cardiomyopathy. Furthermore, current open questions and future challenges in investigating striated muscle nuclear mechanosignaling are further discussed.

【 授权许可】

Unknown   
Copyright © 2023 Zhang, Powers, McCulloch and Chi.