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MeSH Review

Myocytes, Cardiac

 
 
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Disease relevance of Myocytes, Cardiac

 

High impact information on Myocytes, Cardiac

  • Interestingly, HERG current is not blocked by drugs that specifically block IKr in cardiac myocytes [6].
  • This pH-sensitive 'histidine button' engineered in TnI produces a titratable molecular switch that 'senses' changes in the intracellular milieu of the cardiac myocyte and responds by preferentially augmenting acute and long-term function under pathophysiological conditions [7].
  • In cultures of cardiac myocytes, adiponectin activated AMPK and inhibited agonist-stimulated hypertrophy and ERK activation [8].
  • Adenoviral gene transfer of dominant-negative or wild-type PKC-alpha into cardiac myocytes enhances or reduces contractility, respectively [9].
  • Transplantation of 5 x 10(6) cells overexpressing Akt into the ischemic rat myocardium inhibited the process of cardiac remodeling by reducing intramyocardial inflammation, collagen deposition and cardiac myocyte hypertrophy, regenerated 80-90% of lost myocardial volume, and completely normalized systolic and diastolic cardiac function [10].
 

Chemical compound and disease context of Myocytes, Cardiac

 

Biological context of Myocytes, Cardiac

 

Anatomical context of Myocytes, Cardiac

 

Associations of Myocytes, Cardiac with chemical compounds

 

Gene context of Myocytes, Cardiac

 

Analytical, diagnostic and therapeutic context of Myocytes, Cardiac

References

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  18. Reactive oxygen species (ROS)-induced ROS release: a new phenomenon accompanying induction of the mitochondrial permeability transition in cardiac myocytes. Zorov, D.B., Filburn, C.R., Klotz, L.O., Zweier, J.L., Sollott, S.J. J. Exp. Med. (2000) [Pubmed]
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