A Thermodynamic Model of Biological Body: Muscle Mechanics

1978 ◽  
Vol 100 (1) ◽  
pp. 14-19 ◽  
Author(s):  
G. Brankov ◽  
N. Petrov
Keyword(s):  
Thermodynamic Model ◽  
Viscoelastic Properties ◽  
Muscle Mechanics ◽  
Active Muscle ◽  
Body Muscle ◽  
Reacting Mixtures ◽  
Chemically Reacting

The paper is an application of the theory of chemically reacting mixtures to the mechanics of active muscle. It is indicated that some empirical rheologic models can be obtained as particular cases. Viscoelastic properties of the tissue are obtained as a result of a relaxation in the binding of actin and miosin molecules.

Heat Transfer in Chemically Reacting Mixtures. I

1957 ◽  
Vol 26 (2) ◽  
pp. 274-281 ◽  
Author(s):  
Joseph O. Hirschfelder
Keyword(s):  
Heat Transfer ◽  
Reacting Mixtures ◽  
Chemically Reacting

scholarly journals N2A Titin: Signaling Hub and Mechanical Switch in Skeletal Muscle

2020 ◽  
Vol 21 (11) ◽  
pp. 3974 ◽  
Author(s):  
Kiisa Nishikawa ◽  
Stan L. Lindstedt ◽  
Anthony Hessel ◽  
Dhruv Mishra
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mechanics ◽  
Active Muscle ◽  
Small Deletion ◽  
Calcium Dependent ◽  
Hypertrophic Signaling ◽  
Pevk Region ◽  
Mechanical Switch ◽  
The Impact ◽  
Muscle Calcium

Since its belated discovery, our understanding of the giant protein titin has grown exponentially from its humble beginning as a sarcomeric scaffold to recent recognition of its critical mechanical and signaling functions in active muscle. One uniquely useful model to unravel titin’s functions, muscular dystrophy with myositis (mdm), arose spontaneously in mice as a transposon-like LINE repeat insertion that results in a small deletion in the N2A region of titin. This small deletion profoundly affects hypertrophic signaling and muscle mechanics, thereby providing insights into the function of this specific region and the consequences of its dysfunction. The impact of this mutation is profound, affecting diverse aspects of the phenotype including muscle mechanics, developmental hypertrophy, and thermoregulation. In this review, we explore accumulating evidence that points to the N2A region of titin as a dynamic “switch” that is critical for both mechanical and signaling functions in skeletal muscle. Calcium-dependent binding of N2A titin to actin filaments triggers a cascade of changes in titin that affect mechanical properties such as elastic energy storage and return, as well as hypertrophic signaling. The mdm phenotype also points to the existence of as yet unidentified signaling pathways for muscle hypertrophy and thermoregulation, likely involving titin’s PEVK region as well as the N2A signalosome.

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