Alpha-lipoic acid attenuates cardiac hypertrophy via downregulation of PARP-2 and subsequent activation of SIRT-1

Zhang, Lan; Zou, Jian; Chai, Erqing; Qi, Yongmei; Zhang, Yingmei

doi:10.1016/j.ejphar.2014.09.037

Cited by 22 publications

(20 citation statements)

References 33 publications

(27 reference statements)

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“…Low PARP2 expression or the loss of PARP2 induced a phenotype characterized by lipidome changes and improved muscular contractile function. A recent study showed that α-lipoic acid downregulates PARP2 expression [33], suggesting that lipidmediated regulatory circles may include changes in PARP2 expression. Lipids frequently exert their expression effects through nuclear receptors; therefore, we assessed the existing…”

Section: Lipids Can Modulate the Expression Of Parp2mentioning

confidence: 99%

“…The current study suggests that certain lipids can repress the expression of PARP2 and, therefore, PARP2 protein levels and activity. The first lipid species shown to inhibit PARP2 expression was α-lipoic acid [33]. Importantly, decreased PARP2 expression via α-lipoic acid had functional consequences, including enhanced SIRT1 activation [33].…”

Section: Srebp1-dependent Increases In Cholesterol Content Upon Decrementioning

confidence: 99%

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Poly(ADP-ribose) polymerase-2 is a lipid-modulated modulator of muscular lipid homeostasis

Marton

Péter

Balogh

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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There is a growing body of evidence that poly(ADP-ribose) polymerase-2 (PARP2), although originally described as a DNA repair protein, has a widespread role as a metabolic regulator. We show that the ablation of PARP2 induced characteristic changes in the lipidome. The silencing of PARP2 induced the expression of sterol regulatory element-binding protein-1 and -2 and initiated de novo cholesterol biosynthesis in skeletal muscle. Increased muscular cholesterol was shunted to muscular biosynthesis of dihydrotestosterone, an anabolic steroid. Thus, skeletal muscle fibers in PARP2 mice were stronger compared to those of their wild-type littermates. In addition, we detected changes in the dynamics of the cell membrane, suggesting that lipidome changes also affect the biophysical characteristics of the cell membrane. In in silico and wet chemistry studies, we identified lipid species that can decrease the expression of PARP2 and potentially phenocopy the genetic abruption of PARP2, including artificial steroids. In view of these observations, we propose a new role for PARP2 as a lipid-modulated regulator of lipid metabolism.

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Section: Lipids Can Modulate the Expression Of Parp2mentioning

confidence: 99%

Section: Srebp1-dependent Increases In Cholesterol Content Upon Decrementioning

confidence: 99%

Poly(ADP-ribose) polymerase-2 is a lipid-modulated modulator of muscular lipid homeostasis

Marton

Péter

Balogh

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…As a powerful antioxidant, LA can play a physiological role by removing chemical toxicants, scavenging free radicals and reactive oxygen species, inhibiting the production of oxygen free radicals, and improving blood circulation (Zhang et al, 2014;Taneka et al, 2015) (Zhang et al, 2014;Tanaka et al, 2015). Recent research confirmed that it has inhibitory effect on a variety of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of lipoic acid combined with paclitaxel on breast cancer cells

Ren

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Breast cancer is the most common gynecologic tumor globally that threatens women's health. Lipoic acid is a type of antioxidant that can alleviate oxidative stress damage. Studies showed that lipoic acid could inhibit the proliferation of tumor cells in cervical cancer and colon cancer. This paper intends to explore the combined effect of lipoic acid and paclitaxel on breast cancer cells. Breast cancer MCF-7 cells were divided into four groups: control group, lipoic acid group, paclitaxel group, and a combination group. MTT was applied to detect the drugs' influence on breast cancer cell proliferation. A colony formation test was used to determine the effects on breast cancer cell clone formation rate. Western blot was performed to detect the effects on nuclear factor (NF)-κB. Lipoic acid alone can inhibit tumor cell proliferation and clone formation with time dependence. Compared with the control, paclitaxel alone can significantly suppress tumor cell proliferation and clone formation (P < 0.05). Lipoic acid and paclitaxel in combination obviously strengthened their individual inhibitory effects on tumor cells (P < 0.05). Compared with 17935 Lipoic acid combined with paclitaxel on breast cancer ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 17934-17940 (2015) the paclitaxel alone group, the combination group exhibited more remarkable inhibitory effect (P < 0.05). Lipoic acid alone or combined with paclitaxel can inhibit NF-κB expression and inhibit breast cancer cell proliferation.

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“…ALA has a robust anti-hypertrophic and anti-remodeling effect that is mediated by inhibition of C/EBPβ activation [113]. Other authors have suggested that ALA partially attenuates cardiac hypertrophy via inhibition of PPAR2 and subsequent activation of Sirt1 and have proposed that it may have a potential cardio-protective role [112].…”

Section: Strategies To Decrease Factors Inducing Heart Damagementioning

confidence: 99%

New Treatment Strategies for Alcohol-Induced Heart Damage

Fernández‐Solà

Porta

2016

IJMS

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High-dose alcohol misuse induces multiple noxious cardiac effects, including myocyte hypertrophy and necrosis, interstitial fibrosis, decreased ventricular contraction and ventricle enlargement. These effects produce diastolic and systolic ventricular dysfunction leading to congestive heart failure, arrhythmias and an increased death rate. There are multiple, dose-dependent, synchronic and synergistic mechanisms of alcohol-induced cardiac damage. Ethanol alters membrane permeability and composition, interferes with receptors and intracellular transients, induces oxidative, metabolic and energy damage, decreases protein synthesis, excitation-contraction coupling and increases cell apoptosis. In addition, ethanol decreases myocyte protective and repair mechanisms and their regeneration. Although there are diverse different strategies to directly target alcohol-induced heart damage, they are partially effective, and can only be used as support medication in a multidisciplinary approach. Alcohol abstinence is the preferred goal, but control drinking is useful in alcohol-addicted subjects not able to abstain. Correction of nutrition, ionic and vitamin deficiencies and control of alcohol-related systemic organ damage are compulsory. Recently, several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCK inhibitors) and new cardiomyokines such as FGF21 have been described to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms, and they are promising agents in this field. New potential therapeutic targets aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis and persistent apoptosis In addition, stem-cell therapy may improve myocyte regeneration. However, these strategies are not yet approved for clinical use.

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Alpha-lipoic acid attenuates cardiac hypertrophy via downregulation of PARP-2 and subsequent activation of SIRT-1

Cited by 22 publications

References 33 publications

Poly(ADP-ribose) polymerase-2 is a lipid-modulated modulator of muscular lipid homeostasis

Poly(ADP-ribose) polymerase-2 is a lipid-modulated modulator of muscular lipid homeostasis

Effect of lipoic acid combined with paclitaxel on breast cancer cells

New Treatment Strategies for Alcohol-Induced Heart Damage

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