Involvement of NADPH Oxidases in Cardiac Remodelling and Heart Failure

2007 ◽  
Vol 27 (6) ◽  
pp. 649-660 ◽  
Author(s):  
Alexander Sirker ◽  
Min Zhang ◽  
Colin Murdoch ◽  
Ajay M. Shah
Author(s):  
Artemio García-Escobar ◽  
Santiago Jiménez-Valero ◽  
Guillermo Galeote ◽  
Alfonso Jurado-Román ◽  
Julio García-Rodríguez ◽  
...  

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
D Heinzmann ◽  
K Mueller ◽  
K Klingel ◽  
J Kumbrink ◽  
T Kirchner ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Lingyu Xu ◽  
Joseph Pagano ◽  
Kelvin Chow ◽  
Gavin Y. Oudit ◽  
Mark J. Haykowsky ◽  
...  

2011 ◽  
Vol 25 (3) ◽  
pp. 323-332 ◽  
Author(s):  
Yuehua Fang ◽  
Julie Favre ◽  
Magalie Vercauteren ◽  
Brigitte Laillet ◽  
Isabelle Remy-Jouet ◽  
...  

2019 ◽  
Vol 97 (9) ◽  
pp. 902-908 ◽  
Author(s):  
Ghassan Bkaily ◽  
Wassim Najibeddine ◽  
Danielle Jacques

During the development of heart failure in humans and animal models, an increase in reactive oxygen species (ROS) levels was observed. However, there is no information whether this increase of ROS is associated with an increase in the density of specific isoforms of NADPH oxidases (NOXs) 1–5. The objective of this study was to verify whether the densities of NOXs 1–5 change during the development of heart failure. Using the well-known model of cardiomyopathic hamsters, the UM-X 7.1 line, a model that strongly resembles the pathology observed in humans from a morphological and functional point of view, our studies showed that, as in humans, NOXs 1–5 are present in both normal and UM-X7.1 hamster hearts. Even though the densities of NOXs 2 and 5 were unchanged, the levels of both NOXs 1 and 4 significantly decreased in UM-X7.1 hamster hearts during heart failure. These changes were accompanied with a significant increase in NOX3 level. These results suggest that, during heart failure, NOX3 plays a vital role in compensating the decrease of NOXs 1 and 4. This increase in NOX3 may also be responsible, at least in part, for the reported increase in ROS levels in heart failure.


2020 ◽  
Vol 2020 ◽  
pp. 1-21 ◽  
Author(s):  
Alexander E. Berezin ◽  
Alexander A. Berezin

The prevalence of heart failure (HF) due to cardiac remodelling after acute myocardial infarction (AMI) does not decrease regardless of implementation of new technologies supporting opening culprit coronary artery and solving of ischemia-relating stenosis with primary percutaneous coronary intervention (PCI). Numerous studies have examined the diagnostic and prognostic potencies of circulating cardiac biomarkers in acute coronary syndrome/AMI and heart failure after AMI, and even fewer have depicted the utility of biomarkers in AMI patients undergoing primary PCI. Although complete revascularization at early period of acute coronary syndrome/AMI is an established factor for improved short-term and long-term prognosis and lowered risk of cardiovascular (CV) complications, late adverse cardiac remodelling may be a major risk factor for one-year mortality and postponded heart failure manifestation after PCI with subsequent blood flow resolving in culprit coronary artery. The aim of the review was to focus an attention on circulating biomarker as a promising tool to stratify AMI patients at high risk of poor cardiac recovery and developing HF after successful PCI. The main consideration affects biomarkers of inflammation, biomechanical myocardial stress, cardiac injury and necrosis, fibrosis, endothelial dysfunction, and vascular reparation. Clinical utilities and predictive modalities of natriuretic peptides, cardiac troponins, galectin 3, soluble suppressor tumorogenicity-2, high-sensitive C-reactive protein, growth differential factor-15, midregional proadrenomedullin, noncoding RNAs, and other biomarkers for adverse cardiac remodelling are discussed in the review.


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