Phospholipase Signalling Pathways in Thyroxine‐Induced Cardiac Hypertrophy<sup>a</sup>

Williams, Sean A.; Mesaeli, Nasrin; Panagia, Vincenzo

doi:10.1111/j.1749-6632.1995.tb17421.x

Cited by 4 publications

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…of the lipid membrane, with subsequent perturbation of membrane-bound enzymes and receptors 6 . In addition, oxidative stress is enhanced in many cardiac diseases such as ischemia-reperfusion, cardiac hypertrophy, catecholamine-induced cardiomyopathy and heart failure 7 .…”

Section: Free Radicals May Affect Cardiac Function Through Various Mementioning

confidence: 99%

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

et al. 2010

View full text Add to dashboard Cite

Vitamin C scavenges toxic free radicals as an antioxidant, and oxidative stress is considered as a major contributor inducing damage to cardiomyocytes in heart diseases. Also, it is well-known that stress provokes oxidative stress and induces cardiac sudden death. Here we show the effects of vitamin C on the prevention of cardiac damage by stress in gulo(-/-) mice which cannot synthesize vitamin C. Vitamin C-insufficient gulo(-/-) mice under stress showed prominent cardiac damage and expired within 2 weeks. It was accompanied with structural changes in the heart, cardiac dysfunction and severe emphysema. These changes were caused by the elevation of pro-inflammatory cytokines, especially TNF-&x03B1;, the activation of MMP-2/MMP-9, an increase in oxidative stress and a remarkable decrease in noradrenaline production. Thus, vitamin C insufficiency causes extensive cardiac damage under stress through regulating cytokine and hormone production as well as redox homeostasis, which results in stress-induced sudden death.

show abstract

Section: Free Radicals May Affect Cardiac Function Through Various Mementioning

confidence: 99%

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

et al. 2010

View full text Add to dashboard Cite

show abstract

“…However, little has been known about the effect of hypothyroidism on DAG content in cells. It has been demonstrated that activity of PLC and PLD was depressed [ 10 ], and DAG level decreased [ 11 ] in thyroxine-induced cardiac hypertrophy. In contrast, experimental hyperthyroidism caused a significant increase in inositol trisphosphate formation and PLC activation in the perfused hearts while hypothyroidism was associated with a decrease in this activity [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Drug-induced and postnatal hypothyroidism impairs the accumulation of diacylglycerol in liver and liver cell plasma membranes

Krasilnikova¹,

Kavok²,

Babenko³

2002

BMC Physiol

View full text Add to dashboard Cite

Background: Thyroid hormones are well known modulators of signal transduction. The effect of hyper-and hypo-thyroidism on diacylglycerol/protein kinase C (DAG/PKC) signaling in cardiomiocytes has been determined. Triiodothyronine (T 3 ) has been shown to prevent the α1-adrenoreceptor-mediated activation of PKC but does not alter the stimulation of enzyme and hepatic metabolism by phorbol ethers. It has been suggested that the elevation of endogenous DAG in senescent or hypothyroid cells changes the PKC-dependent response of cells to phorbol esters and hormones. In the present study, was examined the formation of DAG and activation of PKC in liver cells from rats of different thyroid status.

show abstract

Vitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-α, and ROS production in Gulo(−/−) mice

Kim

Bae

Kim

et al. 2013

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Phospholipase Signalling Pathways in Thyroxine‐Induced Cardiac Hypertrophy^a

Cited by 4 publications

References 19 publications

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

Drug-induced and postnatal hypothyroidism impairs the accumulation of diacylglycerol in liver and liver cell plasma membranes

Vitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-α, and ROS production in Gulo(−/−) mice

Contact Info

Product

Resources

About

Phospholipase Signalling Pathways in Thyroxine‐Induced Cardiac Hypertrophya

Cited by 4 publications

References 19 publications

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

Vitamin C insufficiency causes the stress-induced sudden death through the induction of extensive heart injury.

Drug-induced and postnatal hypothyroidism impairs the accumulation of diacylglycerol in liver and liver cell plasma membranes

Vitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-α, and ROS production in Gulo(−/−) mice

Contact Info

Product

Resources

About

Phospholipase Signalling Pathways in Thyroxine‐Induced Cardiac Hypertrophy^a