A TRiP to heart failure.

@article{Vennekens2013ATT,
  title={A TRiP to heart failure.},
  author={R. Vennekens},
  journal={Cardiovascular research},
  year={2013},
  volume={99 4},
  pages={
          590-1
        }
}
  • R. Vennekens
  • Published 2013
  • Chemistry, Medicine
  • Cardiovascular research
This editorial refers to ‘Blockade of sarcolemmal TRPV2 accumulation inhibits progression of dilated cardiomyopathy’ by Y. Iwata et al ., pp. 757–765, this issue. Transient receptor potential (TRP) channels constitute a somewhat eclectic family of ion channels that share structural similarities and some functional properties, especially cation permeability and weak voltage sensitivity. TRP channels are expressed in virtually every cell type present in the heart, including cardiomyocytes… Expand
1 Citations
Stretch-activated TRPV2 channels: Role in mediating cardiopathies.
TLDR
An overview of the current literature and concepts of TRPV2 channels involvement in the mechanical coupling mechanisms in heart and in the mechanisms that lead to cardiomyopathies leads us to think that TRpV2 may also be an important cardiac drug target based on its major physiological roles in heart. Expand

References

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TLDR
Sarcolemmal TRPV2 accumulation appears to have considerable pathological impact on DCM progression, and blockade of this channel may be a promising therapeutic strategy for treating advanced heart failure. Expand
TRPC Channels As Effectors of Cardiac Hypertrophy
TLDR
The emerging evidence that TRP channels, especially TRPCs, are critical regulators of microdomain signaling in the heart to control pathological hypertrophy in coordination with signaling through effectors such as calcineurin and NFAT is reviewed. Expand
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TLDR
It is proposed that the response to probenecid is due to activation of TRPV2 channels secondary to SR release of Ca(2+) handling and β-adrenergic signaling pathway proteins, which showed that the contractility was not increased through activation of the β-ADR. Expand
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Trpm7 is dispensable in adult ventricular myocardium under basal conditions but is critical for myocardial proliferation during early cardiogenesis, and loss of Trpm7 at an intermediate developmental time point alters theMyocardial transcriptional profile in adulthood, impairing ventricular function, conduction, and repolarization. Expand
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TLDR
Analysis of the properties of myotubes prepared from δ-sarcoglycan–deficient BIO14.6 hamsters revealed that GRC is activated in response to myocyte stretch and is responsible for enhanced Ca2+ influx and resultant cell damage as measured by creatine phosphokinase efflux, suggesting that G RC is a key player in the pathogenesis of myocyte degeneration caused by dystrophin–glycoprotein complex disruption. Expand
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The presented results underscore the role of TRP channels in cardiomyocytes, smooth cells and endothelium, and in disease states such as hypertension, cardiac conduction block and cardiac hypertrophy. Expand
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TLDR
Although initially characterized as a noxious heat sensor, TRPV2 now seems to have little to do with temperature sensing but a much more complex physiological profile, and the available information and research progress on the structure, physiology and pharmacology of TRpV2 are reviewed in an attempt to shed some light on the physiological and pharmacological deorphanization. Expand
What do we know about the Transient Receptor Potential Vanilloid 2 ( TRPV 2 ) ion channel ?
Transient receptor potential (TRP) ion channels are emerging as a new set of membrane proteins involved in a vast array of cellular processes and regulated by a large number of physical and chemicalExpand
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TLDR
TRPV2 is regulated by insulin and is involved in the autocrine action of this hormone on β-cells, and knockdown of TRPV 2 reduced insulin secretion induced by glucose. Expand
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