The Adenine Nucleotide Translocator: Regulation And Function During Myocardial Development And Hypertrophy

@article{Portman2002TheAN,
  title={The Adenine Nucleotide Translocator: Regulation And Function During Myocardial Development And Hypertrophy},
  author={Michael A. Portman},
  journal={Clinical and Experimental Pharmacology and Physiology},
  year={2002},
  volume={29}
}
  • M. Portman
  • Published 1 April 2002
  • Biology
  • Clinical and Experimental Pharmacology and Physiology
1. The present review focuses on the adenine nucleotide translocator (ANT), which facilitates exchange of cytosolic ADP for mitochondrial ATP. This protein serves a central role in regulating cellular oxidative capacity. 
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Direct functional interplay exists in cardiomyocytes between mitochondria and other subcellular compartments that makes it possible direct energy and signal channeling between organelles.
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TLDR
Cardiomyocyte‐restricted overexpression of ANT1 prevents the development of diabetic cardiomyopathy; therefore, accelerated ADP/ATP exchange could be a new promising target to treat diabetic carduomyopathy.
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TLDR
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Cardiac Metabolic Changes in Altered Thyroid States
TLDR
Clinical studies have shown that thyroid hormone supplementation in altered states improves cardiac function, and studies in animal models emulating clinical scenarios with disrupted thyroid homeostasis demonstrate that thyroid supplementation promotes flux through pyruvate dehydrogenase (PDH) in the heart along with preservation of high-energy phosphate reserves and contractile function.
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References

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Thyroid Hormone Coordinates Respiratory Control Maturation and Adenine Nucleotide Translocator Expression in Heart In Vivo
TLDR
Data imply that the maturational shift away from ADP-mediated respiratory control is regulated by thyroid hormone in vivo, and specific thyroid-modulated increases in ANT mRNA and protein imply that this regulation occurs in part at a pretranslational level.
Expression of adenine nucleotide translocator parallels maturation of respiratory control in heart in vivo.
TLDR
Data indicate that respiratory control pattern in the newborn is consistent with a kinetic type regulation through ANT, maturational decreases in control in sheep heart are paralleled by specific increases in ANT content, and regulation of these changes in ANt may be related to increases in steady-state transcript levels for its gene.
Signaling and expression for mitochondrial membrane proteins during left ventricular remodeling and contractile failure after myocardial infarction.
Regulation of adenine nucleotide translocase and glycerol 3-phosphate dehydrogenase expression by thyroid hormones in different rat tissues.
TLDR
It is concluded that the T3-mediated transcriptional induction leading to increased activity of ANT2 and mGPDH contributes considerably to the increase in mitochondrial oxygen consumption in rat tissues.
Myocardial Energetics In Cardiac Hypertrophy
1. This review is presented with the intent of illustrating the representative studies of functional and myocardial energetic consequences of hearts with postinfarction left ventricular (LV)
Expression of the ADP/ATP carrier and expansion of the mitochondrial (ATP + ADP) pool contribute to postnatal maturation of the rat heart.
TLDR
The data strongly indicate that the increase in the AAC activity is an essential step in the postnatal maturation of rat heart mitochondria.
The Signal Transduction Function for Oxidative Phosphorylation Is at Least Second Order in ADP*
To maintain ATP constant in the cell, mitochondria must sense cellular ATP utilization and transduce this demand to F0-F1-ATPase. In spite of a considerable research effort over the past three
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