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Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...
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A material's elastic behavior is characterized by the disappearance of stress once the load is removed, allowing the material to return to its original state. However, when stress surpasses the yield point, yielding commences, marking the onset of plastic deformation or permanent set. This change from elastic to plastic behavior is influenced by the peak stress value and the duration before the load is removed. An intriguing observation occurs when a specimen is loaded, unloaded, and...
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It is essential to understand how structural members behave under plastic deformation when the bending stress exceeds the material's yield strength. This state of deformation permanently alters the shape of the member, in contrast to the linear elastic behavior observed before yielding. The strain at any point in the member is expressed in terms of maximum strain. Notably, the neutral axis, which coincides with the centroid during elastic bending, shifts away from the centroid under plastic...
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Isolation and Cultivation of Adult Rat Cardiomyocytes
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Dyadic Plasticity in Cardiomyocytes.

Peter P Jones1,2, Niall MacQuaide3,4, William E Louch5,6

  • 1Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.

Frontiers in Physiology
|January 9, 2019
PubMed
Summary
This summary is machine-generated.

Cardiomyocyte contraction relies on dyads, specialized junctions between t-tubules and the sarcoplasmic reticulum. Their plasticity, influenced by regulatory proteins, is crucial for cardiac function and disease.

Keywords:
calcium homeostasisdevelopmentdiseasedyadsarcoplasmic reticulumt-tubule

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Area of Science:

  • Cardiovascular Biology
  • Cellular Physiology
  • Molecular Cardiology

Background:

  • Cardiomyocyte contraction depends on dyads, functional junctions between transverse tubules (t-tubules) and the sarcoplasmic reticulum (SR).
  • Dyads regulate calcium (Ca2+) signaling via L-type Ca2+ channels (LTCCs) and Ryanodine Receptors (RyRs), crucial for excitation-contraction coupling.
  • The nanoscale organization within dyads significantly impacts excitation-contraction coupling efficiency.

Purpose of the Study:

  • To review the plasticity of dyadic structures in cardiomyocytes.
  • To highlight the role of regulatory proteins in dyad formation, maintenance, and function.
  • To explore the implications of dyadic plasticity in cardiac health and disease.

Main Methods:

  • Literature review of studies on cardiomyocyte dyads, t-tubules, sarcoplasmic reticulum, LTCCs, and RyRs.
  • Analysis of data on dyad development, remodeling, and degradation.
  • Examination of the roles of junctophilin-2, amphiphysin-2 (BIN1), and caveolin-3 in dyad structure and function.

Main Results:

  • Dyads exhibit remarkable plasticity, forming during development and undergoing remodeling or degradation.
  • Regulatory proteins like junctophilin-2, BIN1, and caveolin-3 are critical for dyadic membrane organization and channel stabilization.
  • Nanoscale clustering of LTCCs and RyRs enables coupled gating, fine-tuning calcium signaling.

Conclusions:

  • Dyadic plasticity is essential for adapting to physiological demands and underlies cardiac compensation and decompensation.
  • Dysfunctional dyads contribute to impaired contractility and arrhythmogenesis in cardiac diseases.
  • Targeting dyadic structure and function offers potential therapeutic strategies for heart disease.