hypertrophy/protease

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A calcium stimulated cysteine protease involved in isoproterenol induced cardiac hypertrophy.

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The purpose of this study was to test the relationship between biochemical and functional changes accompanying beta-agonist induced cardiac hypertrophy and the activation of a calcium stimulated cysteine protease. Because the ultrastructural and ionic changes accompanying beta-agonist induced

Airway smooth muscle enlargement is associated with protease-activated receptor 2/ligand overexpression in patients with difficult-to-control severe asthma.

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Asthma is a complex disease with heterogeneous features of airway inflammation and remodeling. The increase in airway smooth muscle (ASM) mass is an essential component of airway remodeling in patients with severe asthma, yet the pathobiological mechanisms and clinical outcomes associated with ASM

Ubiquitin-specific protease 19 blunts pathological cardiac hypertrophy via inhibition of the TAK1-dependent pathway

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Ubiquitin-specific protease 19 (USP19) belongs to USP family and is involved in promoting skeletal muscle atrophy. Although USP19 is expressed in the heart, the role of USP19 in the heart disease remains unknown. The present study provides in vivo and in vitro data to reveal the role of USP19 in

Protease-activated receptor-1 contributes to cardiac remodeling and hypertrophy.

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BACKGROUND Protease-activated receptor-1 (PAR-1) is the high-affinity receptor for the coagulation protease thrombin. It is expressed by a variety of cell types in the heart, including cardiomyocytes and cardiac fibroblasts. We have shown that tissue factor (TF) and thrombin contribute to infarct

Ubiquitin-Specific Protease 4 Is an Endogenous Negative Regulator of Pathological Cardiac Hypertrophy.

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Dysregulation of the ubiquitin proteasome system components ubiquitin ligases and proteasome plays an important role in the pathogenesis of cardiac hypertrophy. However, little is known about the role of another ubiquitin proteasome system component, the deubiquitinating enzymes, in cardiac

Ubiquitin-specific protease 14 regulates cardiac hypertrophy progression by increasing GSK-3β phosphorylation.

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Cardiac hypertrophy, a compensatory response to various stimuli in the heart, independently predicts cardiovascular ailments and related deaths. Increasing evidence indicates ubiquitin-proteasome signaling contributes to cardiac hypertrophy regulation. Here, we identified ubiquitin-specific protease

Reverse remodeling is associated with changes in extracellular matrix proteases and tissue inhibitors after mesenchymal stem cell (MSC) treatment of pressure overload hypertrophy.

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Changes in ventricular extracellular matrix (ECM) composition of pressure overload hypertrophy determine clinical outcomes. The effects of mesenchymal stem cell (MSC) transplantation upon determinants of ECM composition in pressure overload hypertrophy have not been studied. Sprague-Dawley rats

Maintenance of breast size reduction after mastoplasty and switch to a protease inhibitor-sparing regimen in an HIV-positive woman with highly active antiretroviral therapy-associated massive breast enlargement.

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Fat distribution disorders are among the most frequent side effects of antiretroviral treatment. The pathophysiologic mechanism(s) for these events remains unclear, and a casual link to a specific drug or class of drugs is uncertain. The physical changes associated with the lipodystrophy syndrome

Letter by Strande regarding article "Protease-activated receptor-1 contributes to cardiac remodeling and hypertrophy".

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Breast enlargement with protease inhibitor use.

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Localized adipose tissue hypertrophy in patients receiving human immunodeficiency virus protease inhibitors.

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Myocardial proteases and cardiac remodeling.

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Cardiac hypertrophy (CH), characterized by the enlargement of cardiomyocytes, fibrosis and apoptosis, is one of the leading causes of death worldwide. Despite the advances in cardiovascular research, there remains a need to further investigate the signaling pathways that mediate CH in order to

Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.

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Protease-activated receptor-1 (PAR-1) plays a major role in multiple disease processes, including colitis. Understanding the mechanisms coupling PAR-1 to disease pathogenesis is complicated by the fact that PAR-1 is broadly expressed across multiple cell

Effects of HIV protease inhibitors on progression of monocrotaline- and hypoxia-induced pulmonary hypertension in rats.

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BACKGROUND Pulmonary hypertension (PH) is among the complications of HIV infection. Combination antiretroviral therapy may influence the progression of HIV-related PH. Because Akt signaling is a potential molecular target of HIV protease inhibitors (HPIs), we hypothesized that these drugs altered

Ablation of the stress protease OMA1 protects against heart failure in mice.

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Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. We evaluate three different mouse models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction

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