Category Archives: Circ Res

Genetics of Atrial Fibrillation in 2020: GWAS, Genome Sequencing, Polygenic Risk, and Beyond.

Genetics of Atrial Fibrillation in 2020: GWAS, Genome Sequencing, Polygenic Risk, and Beyond.
Circ Res. 2020 Jun 19;127(1):21-33
Authors: Roselli C, Rienstra M, Ellinor PT
Abstract
Atrial fibrillati… Continue reading

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High-Density Lipoproteins, Endothelial Function, and Mendelian Randomization.

High-Density Lipoproteins, Endothelial Function, and Mendelian Randomization.
Circ Res. 2016 Jun 24;119(1):13-5
Authors: Westerterp M, Wang N, Tall AR
PMID: 27340266 [PubMed – in process]

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The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids.

The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids.
Circ Res. 2015 Sep 10;
Authors: Fu J, Bonder MJ, Cenit MC, Tigchelaar E, Maatman A, Dekens JA, Brandsma E, Marczynska J, Im… Continue reading

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Mitochondrial Reprogramming Induced by CaMKII╬┤ Mediates Hypertrophy Decompensation.

Mitochondrial Reprogramming Induced by CaMKIIδ Mediates Hypertrophy Decompensation.

Circ Res. 2015 Jan 20;

Authors: Westenbrink BD, Ling H, Miyamoto S, Divakaruni A, Gray CB, Zambon AC, Dalton ND, Peterson K, Gu Y, Matkovich SJ, Murphy AN, Dorn GW, Heller Brown J

Abstract
Rationale: Sustained activation of Gq signaling during pressure overload causes cardiac hypertrophy that ultimately progresses to dilated cardiomyopathy. The molecular events that drive hypertrophy decompensation are incompletely understood. Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) is activated downstream of Gq and overexpression of Gq and CaMKIIδ recapitulates hypertrophy decompensation. Objective: To determine whether CaMKIIδ contributes to hypertrophy decompensation provoked by Gq. Methods and Results: Compared to Gαq transgenic (Gq) mice, compound Gq/CaMKIIδ knockout (KO) (Gq/KO) mice developed a similar degree of cardiac hypertrophy but exhibited significantly improved left ventricular function, less cardiac fibrosis and cardiomyocyte apoptosis, and fewer ventricular arrhythmias. Markers of oxidative stress were elevated in mitochondria from Gq vs. WT mice and respiratory rates were lower; these changes in mitochondrial function were restored by CaMKIIδ deletion. Gq-mediated increases in mitochondrial oxidative stress, compromised membrane potential and cell death were recapitulated in NRVMs infected with constitutively active Gq and attenuated by CaMKII inhibition. Deep RNA sequencing revealed altered expression of 41 mitochondrial genes in Gq hearts, with normalization of ~40% of these genes by CaMKIIδ deletion. Uncoupling protein 3 (UCP3) was markedly downregulated in Gq or by Gq expression in NRVMs and reversed by CaMKIIδ deletion or inhibition, as was Peroxisome proliferator-activated receptor alpha (PPAR-α). The protective effects of CaMKIIδ inhibition on ROS generation and cell death were abrogated by knock down of UCP3. Conversely, restoration of UCP3 expression attenuated ROS generation and cell death induced by CaMKIIδ. Our in vivo studies further demonstrated that pressure overload induced decreases in PPAR-α and UCP3, increases in mitochondrial protein oxidation, and hypertrophy decompensation which were attenuated by CaMKIIδ deletion. Conclusions: Mitochondrial gene reprogramming induced by CaMKIIδ emerges as an important mechanism contributing to mitotoxicity in decompensating hypertrophy.

PMID: 25605649 [PubMed – as supplied by publisher]

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Molecular imaging of the cardiac extracellular matrix.

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Molecular imaging of the cardiac extracellular matrix.
Circ Res. 2014 Feb 28;114(5):903-15
Authors: de Haas HJ, Arbustini E, Fuster V, Kramer CM, Narula J
Abstract
In almost all cardi… Continue reading

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Mendelian disorders of high-density lipoprotein metabolism.

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Mendelian disorders of high-density lipoprotein metabolism.
Circ Res. 2014 Jan 3;114(1):124-42
Authors: Oldoni F, Sinke RJ, Kuivenhoven JA
Abstract
High-density lipoproteins (HDLs) are a highly… Continue reading

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Enhanced foam cell formation, atherosclerotic lesion development, and inflammation by combined deletion of ABCA1 and SR-BI in Bone marrow-derived cells in LDL receptor knockout mice on western-type diet.

Enhanced foam cell formation, atherosclerotic lesion development, and inflammation by combined deletion of ABCA1 and SR-BI in Bone marrow-derived cells in LDL receptor knockout mice on western-type diet.
Circ Res. 2010 Dec 10;107(12):e… Continue reading

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