Difference between revisions of "PMID:21409385"

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'''Campbell, KS '''  (2011) Impact of myocyte strain on cardiac myofilament activation. ''Pflugers Arch.'' '''462''':3-14
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!align=left  |Abstract
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When cardiac myocytes are stretched by a longitudinal strain, they develop proportionally more active force at a given sub-maximal Ca(2+) concentration than they did at the shorter length. This is known as length-dependent activation. It is one of the most important contributors to the Frank-Starling relationship, a critical part of normal cardiovascular function. Despite intense research efforts, the mechanistic basis of the Frank-Starling relationship remains unclear. Potential mechanisms involving myofibrillar lattice spacing, titin-based effects, and cooperative activation have all been proposed. This review summarizes some of these mechanisms and discusses two additional potential theories that reflect the effects of localized strains that occur within and between half-sarcomeres. The main conclusion is that the Frank-Starling relationship is probably the integrated result of many interacting molecular mechanisms. Multiscale computational modeling may therefore provide the best way of determining the key processes that underlie length-dependent activation and their relative strengths.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21409385 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3115504 PMC3115504]
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Online version:[http://dx.doi.org/10.1007/s00424-011-0952-3 10.1007/s00424-011-0952-3]
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Actin Cytoskeleton/physiology; Actin Cytoskeleton/ultrastructure; Animals; Calcium/metabolism; Mechanotransduction, Cellular/physiology; Muscle Proteins/metabolism; Myocardial Contraction/physiology; Myocytes, Cardiac/cytology; Myocytes, Cardiac/physiology; Protein Kinases/metabolism; Sarcomeres/physiology; Stress, Mechanical
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==Main Points of the Paper ==
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== Materials and Methods Used ==
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==Phenotype Annotations==
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==Notes==
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==References==
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[[Category:Publication]]

Latest revision as of 18:59, 16 September 2012

Citation

Campbell, KS (2011) Impact of myocyte strain on cardiac myofilament activation. Pflugers Arch. 462:3-14

Abstract

When cardiac myocytes are stretched by a longitudinal strain, they develop proportionally more active force at a given sub-maximal Ca(2+) concentration than they did at the shorter length. This is known as length-dependent activation. It is one of the most important contributors to the Frank-Starling relationship, a critical part of normal cardiovascular function. Despite intense research efforts, the mechanistic basis of the Frank-Starling relationship remains unclear. Potential mechanisms involving myofibrillar lattice spacing, titin-based effects, and cooperative activation have all been proposed. This review summarizes some of these mechanisms and discusses two additional potential theories that reflect the effects of localized strains that occur within and between half-sarcomeres. The main conclusion is that the Frank-Starling relationship is probably the integrated result of many interacting molecular mechanisms. Multiscale computational modeling may therefore provide the best way of determining the key processes that underlie length-dependent activation and their relative strengths.

Links

PubMed PMC3115504 Online version:10.1007/s00424-011-0952-3

Keywords

Actin Cytoskeleton/physiology; Actin Cytoskeleton/ultrastructure; Animals; Calcium/metabolism; Mechanotransduction, Cellular/physiology; Muscle Proteins/metabolism; Myocardial Contraction/physiology; Myocytes, Cardiac/cytology; Myocytes, Cardiac/physiology; Protein Kinases/metabolism; Sarcomeres/physiology; Stress, Mechanical

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Main Points of the Paper

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Materials and Methods Used

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Phenotype Annotations

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Phenotype of Taxon Information Genotype Information (if known) Condition Information OMP ID OMP Term Name ECO ID ECO Term Name Notes Status
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Notes

References

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