Filtered By:
Condition: Cardiomyopathy
This page shows you your search results in order of date. This is page number 11.
Order by Relevance | Date
Total 155 results found since Jan 2013.
Thromboxane A2 Mediates Iron-Overload Cardiomyopathy in Mice Through Calcineurin-Nuclear Factor of Activated T Cells Signaling Pathway.
Conclusions: TXA2 mediates iron-overload cardiomyopathy through the TNF-α-associated calcineurin-NFAT signaling pathway.
PMID: 23856650 [PubMed - as supplied by publisher]
Source: Circulation Journal - July 12, 2013 Category: Cardiology Authors: Lin H, Li HF, Lian WS, Chen HH, Lan YF, Lai PF, Cheng CF Tags: Circ J Source Type: research
O-GlcNAcylation involvement in high glucose-induced cardiac hypertrophy via ERK1/2 and cyclin D2.
In conclusion, O-GlcNAcylation plays a role in high glucose-induced cardiac hypertrophy via ERK1/2 and cyclin D2.
PMID: 23665912 [PubMed - as supplied by publisher]
Source: Amino Acids - May 12, 2013 Category: Biochemistry Authors: Ding F, Yu L, Wang M, Xu S, Xia Q, Fu G Tags: Amino Acids Source Type: research
Cardiomyocyte ryanodine receptor degradation by chaperone-mediated autophagy
Conclusion
These findings are consistent with a model in which oxidative damage of the RyR2 targets it for turnover by presenilins and CMA, which could lead to removal of damaged or leaky RyR2 channels.
Source: Cardiovascular Research - April 23, 2013 Category: Cardiology Authors: Pedrozo, Z., Torrealba, N., Fernandez, C., Gatica, D., Toro, B., Quiroga, C., Rodriguez, A. E., Sanchez, G., Gillette, T. G., Hill, J. A., Donoso, P., Lavandero, S. Tags: ORIGINAL ARTICLES: SPOTLIGHT ON T-TUBULES AND RYANODINE RECEPTOR MICRODOMAIN SIGNALLING IN CARDIAC HYPERTROPHY AND FAILURE Source Type: research
Antioxidant effects of diallyl trisulfide on high glucose-induced apoptosis are mediated by the PI3K/Akt-dependent activation of Nrf2 in cardiomyocytes
Conclusions: Our findings indicate that DATS protects against hyperglycemia-induced ROS-mediated apoptosis by upregulating the PI3K/Akt/Nrf2 pathway, which further activates Nrf2-regulated antioxidant enzymes in cardiomyocytes exposed to HG.
Source: International Journal of Cardiology - March 1, 2013 Category: Cardiology Authors: Cheng-Yen Tsai, Chien-Chung Wang, Tung-Yuan Lai, Han-Nien Tsu, Chung-Hsing Wang, Hsin-Yueh Liang, Wei-Wen Kuo Tags: Original Articles Source Type: research
Determination of the critical residues responsible for cardiac myosin binding protein C's interactions
Abstract: Despite early demonstrations of myosin binding protein C's (MyBP-C) interaction with actin, different investigators have reached different conclusions regarding the relevant and necessary domains mediating this binding. Establishing the detailed structure–function relationships is needed to fully understand cMyBP-C's ability to impact on myofilament contraction as mutations in different domains are causative for familial hypertrophic cardiomyopathy. We defined cMyBP-C's N-terminal structural domains that are necessary or sufficient to mediate interactions with actin and/or the head region of the myosin heavy ch...
Source: Journal of Molecular and Cellular Cardiology - September 13, 2012 Category: Cytology Authors: Md. Shenuarin Bhuiyan, James Gulick, Hanna Osinska, Manish Gupta, Jeffrey Robbins Tags: Original Articles Source Type: research
