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Heart Hypertrophy
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1. Mitochondrial oxidative stress, DNA damage, and heart failure.
Match Strength: 5.679

Recent experimental and clinical studies have suggested that oxidative stress is enhanced in heart failure. The production of oxygen radicals is increased in the failing heart, whereas antioxidant enzyme activities are preserved as normal. Mitochondrial electron transport is an enzymatic source of oxygen radical generation and also a target of oxidant-induced damage. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further oxygen radical generation, and cellular injury. ... Read More »
» Published in Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1737-44.

2. Effects of serum containing Xinlikang on angiotensin ii induced hypertrophy in cultured neonatal rat cardiomyocytes.
Match Strength: 5.498

OBJECTIVE: To evaluate the effects of Xinlikang (XLK) on angiotensin II (Ang II) induced hypertrophic cultured neonatal rat's cardiomyocyte (CMC). METHODS: Primary cultured neonatal rat's CMCs with the purity certified by immunohistochemical technique, were divided into three groups. Rats in the normal control group were untreated; those in the model group were established into hypertrophic models but underwent no treatment; and those in the XLK group were established to hypertrophic models and treated with XLK containing serum obtained from rats with aorta coarctation after 8 days of feeding ... Read More »
» Published in Chin J Integr Med. 2006 Sep;12(3):194-8.

3. The renin-angiotensin system: a therapeutic target in atrial fibrillation.
Match Strength: 4.956

There is growing evidence to suggest a role for the renin-angiotensin system (RAS) in the pathogenesis of atrial fibrillation (AF). Experimental animal data suggest RAS-dependent mechanisms for the development of a structural and electrophysiologic substrate for AF. This is consistent with clinical data demonstrating the effectiveness of RAS blockade in preventing new-onset or recurrent AF in a variety of patient populations including patients with hypertension and left ventricular hypertrophy, congestive heart failure, and those undergoing electrical cardioversion for AF. This review ... Read More »
» Published in Pacing Clin Electrophysiol. 2006 Sep;29(9):1006-12.

4. Activation of Rho-associated coiled-coil protein kinase 1 (ROCK-1) by caspase-3 cleavage plays an essential role in cardiac myocyte apoptosis.
Match Strength: 4.690

Rho-associated coiled-coil protein kinase 1 (ROCK-1) is a direct cleavage substrate of activated caspase-3, which is associated with heart failure. In the course of human heart failure, we found marked cleavage of ROCK-1 resulting in a 130-kDa subspecies, which was absent in normal hearts and in an equivalent cohort of patients with left ventricular assist devices. Murine cardiomyocytes treated with doxorubicin led to enhanced ROCK-1 cleavage and apoptosis, all of which was blocked by a caspase-3 inhibitor. In addition, a bitransgenic mouse model of severe cardiomyopathy, which overexpresses ... Read More »
» Published in Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14495-500. Epub 2006 Sep 18.

5. Thioredoxin1 upregulates mitochondrial proteins related to oxidative phosphorylation and TCA cycle in the heart.
Match Strength: 4.605

Thioredoxin1 (Trx1) inhibits hypertrophy and exhibits protective functions in the heart. To elucidate further the cardiac functions of Trx1, we used a DNA microarray analysis, with hearts from transgenic mice with cardiac- specific overexpression of Trx1 (Tg-Trx1, n = 4) and nontransgenic controls (n = 4). Expression of a large number of genes is regulated in Tg-Trx1, with a greater number of genes downregulated, versus upregulated, at high-fold changes. The peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1gamma) gene was among the top 50 significantly upregulated ... Read More »
» Published in Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1635-50.

6. Prostacyclin therapy increases right ventricular capillarisation in a model for flow-associated pulmonary hypertension.
Match Strength: 3.776

Pulmonary hypertension, and consequently right ventricular failure, complicates several congenital heart defects. Although intervention in the prostacyclin-thromboxane ratio is known to improve outcome, the underlying mechanism is not clear. Therefore, effects of acetyl salicylic acid and iloprost are studied in an animal model for flow-associated pulmonary hypertension. Male Wistar rats with flow-associated pulmonary hypertension, an aortocaval shunt in addition to monocrotaline induced pulmonary hypertension, were treated with low-dose aspirin (25 mg/kg/day) or iloprost (72 microg/kg/day). ... Read More »
» Published in Eur J Pharmacol. 2006 Nov 7;549(1-3):107-16. Epub 2006 Aug 17.

7. Lack of osteopontin improves cardiac function in streptozotocin-induced diabetic mice.
Match Strength: 3.350

The purpose of this study was to investigate the role of osteopontin (OPN) in diabetic hearts. Diabetes was induced in wild-type (WT) and OPN knockout (KO) mice by using streptozotocin (150 mg/kg) injection. Left ventricular (LV) structural and functional remodeling was studied 30 and 60 days after induction of diabetes. Induction of diabetes increased OPN expression in cardiac myocytes. Heart weight-to-body weight ratio was increased in both diabetic (D) groups. Lung wet weight-to-dry weight ratio was increased only in the WT-D group. Peak left ventricular (LV) developed pressures measured ... Read More »
» Published in Am J Physiol Heart Circ Physiol. 2007 Jan;292(1):H673-83. Epub 2006 Sep 15.

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