Resveratrol prevents pathological but not physiological cardiac hypertrophy

Dolinsky, Vernon W.; Soltys, Carrie-Lynn M.; Rogan, Kyle J.; Chan, Anita Y.M.; Nagendran, Jeevan; Wang, Shaohua; Dyck, Jason R.B.

doi:10.1007/s00109-014-1220-8

Cited by 41 publications

(29 citation statements)

References 35 publications

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“…Consistent with previous studies,7, 25 Rev substantially decreased the size of cardiomyocytes. Results from the current study showed that the dosage (10 μmol/L of Rev) markedly reduced the size of cardiomyocytes in vitro (Figure 1).…”

Section: Resultssupporting

confidence: 92%

“…The data from a recent famous study showed that Rev had a markedly inhibitory role on NFAT‐dependent transcription in cardiomyocytes, which suggested that Rev could prevent pathological cardiac hypertrophy by blocking NFAT‐mediated regulation of gene transcription 7. Furthermore, they also showed that Rev could activate AMPK and inhibit Akt signaling in the cardiac myocyte, and these Rev‐mediated effects could inhibit cardiac myocyte hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

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Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Fan

Liu

Fang

et al. 2016

JAHA

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BackgroundThe polyphenol resveratrol (Rev) has been reported to exhibit cardioprotective effects, such as inhibition of TAC (transverse aortic constriction) or isoprenaline (ISO)‐induced hypertrophy. MicroRNA‐155 (miR‐155) was found to be decreased in hypertrophic myocardium, which could be further reduced by pretreatment of Rev. The study was designed to investigate the molecular effects of miR‐155 on cardiac hypertrophy, focusing on the role of breast cancer type 1 susceptibility protein (BRCA1).Methods and ResultsWe demonstrated that Rev alleviated severity of hypertrophic myocardium in a mice model of cardiac hypertrophy by TAC treatment. Down‐regulation of miR‐155 was observed in pressure overload– or ISO‐induced hypertrophic cardiomyoctyes. Interestingly, administration of Rev substantially attenuated miR‐155 level in cardiomyocytes. In agreement with its miR‐155 reducing effect, Rev relieved cardiac hypertrophy and restored cardiac function by activation of BRCA1 in cardiomyoctyes. Our results further revealed that forkhead box O3a (FoxO3a) was a miR‐155 target in the heart. And miR‐155 directly repressed FoxO3a, whose expression was mitigated in miR‐155 agomir and mimic treatment in vivo and in vitro.ConclusionsWe conclude that BRCA1 inactivation can increase expression of miR‐155, contributing to cardiac hypertrophy. And Rev produces their beneficial effects partially by down‐regulating miR‐155 expression, which might be a novel strategy for treatment of cardiac hypertrophy.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Fan

Liu

Fang

et al. 2016

JAHA

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“…Fasudil is the only ROCK inhibitor approved for human use at present, although its specific effect has not been evaluated at a cardiac level [53]. Resveratrol and pioglitazone have relevant antioxidant cardiac properties and have also been suggested to inhibit cardiac hypertrophy [54,55].…”

Section: Future Perspectivesmentioning

confidence: 99%

Alcoholic Cardiomyopathy: Old and New Insights

Fernández‐Solà¹,

Riba²

2017

J Alcohol Drug Depend

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Alcohol cardiomyopathy (ACM) is a chronic dilated heart disease with decreased left ventricular ejection fraction that may be detected in one-fourth of high-dose alcohol consumers. It causes progressive diastolic and systolic dysfunction, supra and ventricular arrhythmias leading to heart failure and increased mortality. The main etiological factor for ACM is ethanol consumption that affects the myocardium in a dose-dependent manner. The mechanisms of ACM are diverse, synchronic and synergistic. Alcohol alters the channel and receptor structure of the cell membrane, decreases intracellular calcium transients, increases oxidative and inflammatory damage, decreases structural protein synthesis and interferes with excitation-contraction coupling mechanisms. Subjects with excessive alcohol consumption may have a subclinical cardiomyopathy with atrial and LV diastolic dysfunction measured by echocardiography or cardiac MR. Subclinical LV dysfunction may progress and later appear clinical features of heart failure. Cardiac myocytes adapt to ethanol aggression by cell and nuclear hypertrophy and dilatation of heart chambers. Progressive myocyte structure disarray and apoptosis produce myocyte loss, hypertrophy of the remaining cells, subendocardial and interstitial fibrosis and low-degree myocyte regeneration. In addition, ethanol also interferes with cardiac repair and adaptation mechanisms. Thus, local cardiomyokines (FGF-21) and growth factors (myostatin, IGF-1, leptin) are modified by ethanol, limiting cardiac remodeling and myocyte regeneration, and leading to abnormal hypertrophy and eccentric ventricle dilatation. This imbalance between aggression and protection mechanisms induces progressive myocyte loss and heart dysfunction. Alcohol abstention is the main goal in ACM, although control drinking (<-60 g/day) may allow recovery of LV function. Monitoring of systemic mediated alcohol-damage, and correction of vitamin and ion deficiencies is needed. Heart failure in ACM should be treated similar to other dilated cardiomyopathies. Heart transplantation is limited to subjects without other organ damage who are able to abstain from alcohol. New preventive and therapeutic strategies are under development to decrease alcohol-mediated myocyte damage and increase heart protective and repair mechanisms.

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“…Resveratrol is one kind of the antioxidant compound and widely exists in peanuts, berries, grapes and some China herbs [16][17][18]. Recently, more and more studies uncover that Resveratrol has anticancer actions on a variety of cancers [19].…”

Section: Introductionmentioning

confidence: 99%

“…Besides, Resveratrol can protect hearts against cardiovascular diseases. For example, Resveratrol was shown to suppress left ventricular hypertrophy and heart failure [17,22]. Resveratrol treatment also inhibits ischemia/reperfusion injury and ventricular arrhythmias [23].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Attenuated Low Ambient Temperature-Induced Myocardial Hypertrophy via Inhibiting Cardiomyocyte Apoptosis

Yin

Zhao

Feng

et al. 2015

Cell Physiol Biochem

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Background/Aims: Low ambient temperature is an important risk factor for cardiovascular diseases, and has been shown to lead to cardiac hypertrophy. In this study, we aim to investigate if Resveratrol may inhibit cold exposure-induced cardiac hypertrophy in mice, and if so to clarify its molecular mechanism. Methods: Adult male mice were randomly assigned to Control group (kept at room temperature), Cold group (kept at low air temperature range from 3°C to 5°C) and Resveratrol treatment group (100mg/kg/day) for eight weeks. HE staining, Masson staining and Transmission electron microscopy were employed to detect cardiac structure, fibrosis and myocardial ultrastructure, respectively. Echocardiogram was used to measure myocardial functions. Western blot was used to detect the expression of MAPK pathway and apoptotic proteins. TUENL assay was performed to evaluate cardiomyocyte apoptosis. qRT-PCR was employed to measure the mRNA level. Results: Cold-treated mice showed a higher heart/body weight ratio and heart weight/tibia length ratio compared with control mice, and Resveratrol treatment may suppress these changes in cold-treated mice. Myocardial cross-section area and cardiac collagen volume were larger in cold group than control group, which also can be attenuated by Resveratrol treatment. Also, Resveratrol improved the ultrastructure damage of myocardium such as myofibril disarray in cold group. Echocardiogram measurement showed that EF and FS values in cold group declined apparently as compared to control group, and Resveratrol may improve the reduction of heart functions. The expression of p-JNK, p-p38 and p-ERK relative to total JNK, p38 and ERK in cold group was not altered in cold group and Resveratrol group as compared to control group. Cold-treated mouse hearts also showed the upregulation of hypertrophy-related miRNA-miR-328 but not miR-23a, and Resveratrol treatment can inhibit the increase of miR-328. Finally, Resveratrol treatment also may suppress apoptosis of myocardium in cold-treated mouse hearts via inhibiting Bax and caspase-3 activation. Conclusion: In summary, low ambient temperature can cause enlarged heart, ultrastructure damage of myocardium and weakened functions, and Resveratrol treatment effectively suppressed these changes at least partially via inhibiting cardiomyocyte apoptosis.

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Resveratrol prevents pathological but not physiological cardiac hypertrophy

Cited by 41 publications

References 35 publications

Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Alcoholic Cardiomyopathy: Old and New Insights

Resveratrol Attenuated Low Ambient Temperature-Induced Myocardial Hypertrophy via Inhibiting Cardiomyocyte Apoptosis

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