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Updated: Jul 16, 2025
Combining 3D Magnetic Force Actuator and Multi-Functional Fluorescence Imaging to Study Nucleus Mechanobiology
Published on: July 5, 2022
Nucleus Mechanosensing in Cardiomyocytes
Isabella Leite Coscarella1, Maicon Landim-Vieira1, Hosna Rastegarpouyani2,3
1Department of Biomedical Sciences, Florida State University, Tallahassee, FL 32306, USA.
Insights
Cardiac cells sense mechanical signals, transmitting them to the nucleus to alter gene expression and cell structure. This mechanotransduction process is crucial for understanding heart disease progression.
Area of Science:
- Cardiology
- Cell Biology
- Biophysics
Background:
- Cardiac muscle contraction relies on actin-myosin interactions modulated by calcium ions.
- Genetic variations in sarcomeric proteins can precipitate cardiac dysfunction.
- The cardiomyocyte's cytoskeleton, including actin filaments, microtubules, and desmin, links sarcomeres to other cellular components.
Purpose of the Study:
- To review the key mechanisms of mechanotransduction in cardiomyocytes.
- To explore how mechanical signals are transmitted from sarcomeres to the nucleus.
- To understand how this signaling impacts gene expression and nuclear morphology.
Main Methods:
- This review synthesizes existing research on cardiomyocyte mechanotransduction.
- It examines the molecular pathways involved in signal transmission.
- It discusses the role of cytoskeletal connections and nuclear envelope proteins.
Main Results:
- Mechanical and biochemical signals from sarcomeric contractions are relayed throughout the cardiomyocyte.
- These signals are sensed by the nucleus, leading to changes in gene expression and nuclear structure.
- Proteins on the nuclear envelope play a significant role in responding to these mechanical stimuli.
Conclusions:
- Mechanotransduction in cardiomyocytes links mechanical forces to nuclear responses, influencing cell behavior.
- Understanding nucleus sensing in conjunction with sarcomeric protein dysfunction aids in comprehending cardiomyopathies.
- This process is vital for adapting to physiological demands and understanding disease pathogenesis.
Abstract:
Cardiac muscle contraction is distinct from the contraction of other muscle types. The heart continuously undergoes contraction-relaxation cycles throughout an animal's lifespan. It must respond to constantly varying physical and energetic burdens over the short term on a beat-to-beat basis and relies on different mechanisms over the long term. Muscle contractility is based on actin and myosin interactions that are regulated by cytoplasmic calcium ions. Genetic variants of sarcomeric proteins can lead to the pathophysiological development of cardiac dysfunction. The sarcomere is physically connected to other cytoskeletal components. Actin filaments, microtubules and desmin proteins are responsible for these interactions. Therefore, mechanical as well as biochemical signals from sarcomeric contractions are transmitted to and sensed by other parts of the cardiomyocyte, particularly the nucleus which can respond to these stimuli. Proteins anchored to the nuclear envelope display a broad response which remodels the structure of the nucleus. In this review, we examine the central aspects of mechanotransduction in the cardiomyocyte where the transmission of mechanical signals to the nucleus can result in changes in gene expression and nucleus morphology. The correlation of nucleus sensing and dysfunction of sarcomeric proteins may assist the understanding of a wide range of functional responses in the progress of cardiomyopathic diseases.
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