Impaired Myocardial Bioenergetics in HFpEF and the Role of Antioxidants

Hiebert, John M.; Shen, Qiuhua; Thimmesch, Amanda R.; Pierce, Janet D.

doi:10.2174/1874192401610010158

Cited by 11 publications

(6 citation statements)

References 34 publications

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“…Energy metabolism is central and the most important function in more metabolically active tissues, such as heart and brain. , Glucose aerobic metabolism plays a potential role in ATP production and maintains diverse biochemical processes in cardiomyocytes and neurons. , Epidemiological, clinical, and experimental evidence strongly supports that impaired bioenergetics generally occurs in myocardial and cerebral ischemia diseases and subsequent reperfusion injuries. − Undoubtedly, the enhancement of energy metabolism has been a potential strategy for improving physical endurance and reducing pathological injury to protect cardiac and neuronal functions.…”

Section: Introductionmentioning

confidence: 99%

A SIRT1 Activator, Ginsenoside Rc, Promotes Energy Metabolism in Cardiomyocytes and Neurons

Huang¹,

Su²,

Qi³

et al. 2021

J. Am. Chem. Soc.

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Targeting SIRT1 signaling pathway could improve glucose aerobic metabolism and mitochondrial biosynthesis to resist cardiac and neurological injuries. Ginsenoside Rc has been identified for targeting mitochondrial function, but how ginsenoside Rc interacts with SIRT1 to regulate energy metabolism in cardiomyocytes and neurons under physiological or ischemia/reperfusion (I/R)-injured conditions has not been clearly investigated. Here, we confirm the interaction of Rc on the residue sites of SIRT1 in promoting its activity. Ginsenoside Rc significantly promotes mitochondrial biogenesis and increases the levels of electron-transport chain complex II–IV in cardiomyocytes and neurons. Meanwhile, ginsenoside Rc pretreatment increases ATP production, glucose uptake, and the levels of hexokinase I/II and mitochondrial pyruvate carrier I/II in both cell models. In addition, ginsenoside Rc activates the PGC1α pathway to induce mitochondrial biosynthesis. More importantly, ginsenoside Rc reduces mitochondrial damage and apoptosis through SIRT1 restoration-mediated reduction of PGC1α acetylation in the I/R-induced cardiac and neuronal models. Collectively, the in vitro and in vivo data indicate that ginsenoside Rc as a SIRT1 activator promotes energy metabolism to improve cardio- and neuroprotective functions under normal and I/R injury conditions, which provides new insights into the molecular mechanism of ginsenoside Rc as a protective agent.

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Section: Introductionmentioning

confidence: 99%

A SIRT1 Activator, Ginsenoside Rc, Promotes Energy Metabolism in Cardiomyocytes and Neurons

Huang¹,

Su²,

Qi³

et al. 2021

J. Am. Chem. Soc.

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“…Microvascular inflammation, endothelial activation, reduction in nitric oxide, adenosine triphosphate, and cyclic guanosine monophosphate all together lead to microvascular ischemia, LV remodeling, and fibrosis. [ 31 , 32 ] Medications (e.g., chloroquine and hydroxychloroquine) used for long term in patients with SLE causes deficiency in lysosomal cells that lead to intracellular accumulation of glycogen and membrane phospholipids, inducing cardiac structural and functional abnormalities and possibly leading to HF. [ 33 ] Moreover, thrombotic microvasculopathy, attributed to antiphospholipid antibodies, is responsible for myocardial ischemia, even in the absence of obstructive CAD.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular systolic function assessed by standard and advanced echocardiographic techniques in patients with systemic lupus erythematosus: A systemic review and meta-analysis

Gegenava,

Kirtava,

Kong

et al. 2024

Arch Rheumatol

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Objectives: Aim of the study was to perform a systemic review and meta-analysis of the current case-control studies based on the assessment of the left ventricular (LV) systolic function with standard and advanced echocardiographic methods. Materials and methods: Objectives of the study, methods of statisticalanalysis, literature search strategy, inclusion andexclusion criteria, and outcome measurementswere defined according to Cochrane Collaborationsteps, 13 including recommendations for metaanalysisof observational studies in epidemiology (MOOSE). Results: A total of 850 papers were collected. Of those, eight papers (10 groups) including 174,442 SLE patients and 45,608,723 controls with heart failure (HF), 20 papers including 1,121 SLE patients and 1,010 controls with an evaluated LV ejection fraction (LVEF), and eight studies (nine groups) including 462 SLE patients and 356 controls with a measured LV global longitudinal strain (LVGLS) met the predefined inclusion criteria. HF rate in SLE patients was 2.39% (4,176 of 174,442 patients with HF), and SLE patients showed a 3.4 times higher risk for HF compared to controls. SLE patients had a lower LVEF compared to controls. LVGLS was more impaired in SLE patients compared to controls, irrespective of two-dimensional or three-dimensional speckle tracking echocardiography. Conclusion: Heart failure rate in SLE patients is high, and SLE patients showed a 3.4 times higher risk in patients with SLE compared to controls. LV systolic function, as measured by LVEF and LVGLS, is significantly affected in SLE patients, and LVGLS potentially represents a new tool for the early assessment of LV function.

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“…The importance of Q10, L -arginine, and VD alone on the cardiovascular system is well known. Q10 is an integral component of the mitochondrial respiratory chain for ATP production as well as an antioxidant agent, thus it could assist in improving myocardial function in HF patients [52]. In addition, a meta-analysis on coenzyme Q10 randomized clinical trials showed that it improves the outcomes of HF patients.…”

Section: Discussionmentioning

confidence: 99%

Cooperative Effects of Q10, Vitamin D<sub>3</sub>, and <smlcap>L</smlcap>-Arginine on Cardiac and Endothelial Cells

et al. 2018

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This work demonstrates the cooperative effect of Q10, vitamin D_3, and L-arginine on both cardiac and endothelial cells. The effects of Q10, L-arginine, and vitamin D₃ alone or combined on cell viability, nitric oxide, and reactive oxygen species productions in endothelial and cardiac cells were studied. Moreover, the involvement of PI3K/Akt and ERK/MAPK pathways leading to eNOS activation as well as the involvement of vitamin D receptor were also investigated. The same agents were tested in an animal model to verify vasodilation, nitric oxide, and reactive oxygen species production. The data obtained in this work demonstrate for the first time the beneficial and cooperative effect of stimulation with Q10, L-arginine, and vitamin D₃. Indeed, in cardiac and endothelial cells, Q10, L-arginine, and vitamin D₃ combined were able to induce a nitric oxide production higher than the that induced by the 3 substances alone. The effects on vasodilation induced by cooperative stimulation have been confirmed in an in vivo model as well. The use of a combination of Q10, L-arginine, and vitamin D to counteract increased free radical production could be a potential method to reduce myocardial injury or the effects of aging on the heart.

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Impaired Myocardial Bioenergetics in HFpEF and the Role of Antioxidants

Cited by 11 publications

References 34 publications

A SIRT1 Activator, Ginsenoside Rc, Promotes Energy Metabolism in Cardiomyocytes and Neurons

A SIRT1 Activator, Ginsenoside Rc, Promotes Energy Metabolism in Cardiomyocytes and Neurons

Left ventricular systolic function assessed by standard and advanced echocardiographic techniques in patients with systemic lupus erythematosus: A systemic review and meta-analysis

Cooperative Effects of Q10, Vitamin D<sub>3</sub>, and <smlcap>L</smlcap>-Arginine on Cardiac and Endothelial Cells

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