2013
DOI: 10.1161/circresaha.113.301684
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Exercise Training in Patients with Chronic Heart Failure Promotes Restoration of High-Density Lipoprotein Functional Properties

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Cited by 71 publications
(81 citation statements)
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“…24 Activation of PKC-bII inhibits Akt-dependent eNOS from activating phosphorylation at Ser1177, and promotes phosphorylation of eNOS at Thr495, which leads to decreased eNOS activity. 25,26 Activation of p70S6K, the downstream target of PKC-bII, was considered to be activating phosphorylation of eNOS at the inhibitory site Thr495. 26 Taken together, MPs from VHD patients could inhibit eNOS activation and reduce nitric oxide generation via inhibition of the Akt-eNOS pathway, the activation of the PKC-bII/p70S6K-eNOS pathway, and increased expression of caveolin-1.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…24 Activation of PKC-bII inhibits Akt-dependent eNOS from activating phosphorylation at Ser1177, and promotes phosphorylation of eNOS at Thr495, which leads to decreased eNOS activity. 25,26 Activation of p70S6K, the downstream target of PKC-bII, was considered to be activating phosphorylation of eNOS at the inhibitory site Thr495. 26 Taken together, MPs from VHD patients could inhibit eNOS activation and reduce nitric oxide generation via inhibition of the Akt-eNOS pathway, the activation of the PKC-bII/p70S6K-eNOS pathway, and increased expression of caveolin-1.…”
Section: Discussionmentioning
confidence: 99%
“…25,26 Activation of p70S6K, the downstream target of PKC-bII, was considered to be activating phosphorylation of eNOS at the inhibitory site Thr495. 26 Taken together, MPs from VHD patients could inhibit eNOS activation and reduce nitric oxide generation via inhibition of the Akt-eNOS pathway, the activation of the PKC-bII/p70S6K-eNOS pathway, and increased expression of caveolin-1. These findings highlight the harmfulness of MPs in VHD patients, especially after cardiac surgery, for negative regulation of eNOS.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, HDL from patients with either stable CAD or an ACS, in contrast to HDL from age-and gender-matched healthy subjects, inhibited endothelial cell NO production and lost the capacity to limit endothelial inflammatory activation as well as to promote endothelial repair in vivo (Besler et al 2011). Interestingly, the capacity to stimulate endothelial NO production could be improved upon exercise training (Adams et al 2013). HDL from patients with CAD and chronic heart failure (CHF) showed an elevated malondialdehyde (MDA) content as compared to HDL from healthy subjects, which may contribute to the impaired endothelial NO production (Besler et al 2011).…”
Section: Impaired Hdl Capacity To Stimulate No Production In Patientsmentioning
confidence: 99%
“…The potential of life style changes is often underestimated when it comes to improving lipid metabolism. A decrease in body weight (in obese subjects) and an increase in physical activity improve the functionality of HDL and decreases the concentration of triglyceride-rich lipoproteins [21]. On the other hand medications that improve HDL functionality will not necessarily result in an increase of plasma HDLcholesterol.…”
Section: Main Textmentioning
confidence: 99%