Fenofibrate ameliorates neural, mechanical, chemical, and electrical alterations in the murine model of heart failure

Dhyani, Neha; Saidullah, Bano; Fahim, Mohammad; Omanwar, Swati

doi:10.1177/0960327119860173

Cited by 11 publications

(9 citation statements)

References 36 publications

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“… 148 found that fenofibrate prevents the transformation of cardiac metabolic substrates in HF model dogs and moderately improves cardiac function. A study showed that fenofibrate promotes fatty acid oxidation in the mitochondria of isoproterenol-induced HF rats, increases myocardial energy metabolism and oxidative stress, and protects heart function 149 . In addition, fenofibrate also reducing aldosterone-induced myocardial hypertrophy, but it may not be related to fatty acid oxidation 150 .…”

Section: Potential Drugs For Reducing Hf By Regulating Energy Metabolismmentioning

confidence: 99%

Energy metabolism disorders and potential therapeutic drugs in heart failure

Huang

Zhang

et al. 2021

Acta Pharmaceutica Sinica B

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Heart failure (HF) is a global public health problem with high morbidity and mortality. A large number of studies have shown that HF is caused by severe energy metabolism disorders, which result in an insufficient heart energy supply. This deficiency causes cardiac pump dysfunction and systemic energy metabolism failure, which determine the development of HF and recovery of heart. Current HF therapy acts by reducing heart rate and cardiac preload and afterload, treating the HF symptomatically or delaying development of the disease. Drugs aimed at cardiac energy metabolism have not yet been developed. In this review, we outline the main characteristics of cardiac energy metabolism in healthy hearts, changes in metabolism during HF, and related pathways and targets of energy metabolism. Finally, we discuss drugs that improve cardiac function via energy metabolism to provide new research ideas for the development and application of drugs for treating HF.

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Section: Potential Drugs For Reducing Hf By Regulating Energy Metabolismmentioning

confidence: 99%

Energy metabolism disorders and potential therapeutic drugs in heart failure

Huang

Zhang

et al. 2021

Acta Pharmaceutica Sinica B

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“…Furthermore, PPARα-deficient mice are more prone to cardiac hypertrophy in response to pressure overload ( Smeets et al, 2008 ; Wu et al, 2019 ; Wang et al, 2021 ). In addition, PPARα agonist elevates its function to alleviate cardiac hypertrophy ( Kar and Bandyopadhyay, 2018 ; Zeng et al, 2018 ; Dhyani et al, 2019 ). In the present study, salidroside reduced the mRNA expressions of hypertrophic marker ANF and BNP, which indicates that cardiomyocyte hypertrophy induced by Ang II treatment is inhibited.…”

Section: Discussionmentioning

confidence: 99%

“…PPARα is a member of the nuclear receptor family of ligand-activated transcription factors and regulates the uptake, transport and oxidation of fatty acids ( Montaigne et al, 2021 ). The decline of protein expression and transcriptional activity of cardiac PPARα is widely observed in cardiac hypertrophy, and cardiac hypertrophy is enhanced in response to chronic pressure overload in mice of PPARα knockout ( Smeets et al, 2008 ; Wu et al, 2019 ; Wang et al, 2021 ); moreover, PPARα agonists can attenuate cardiac hypertrophy ( Kar and Bandyopadhyay, 2018 ; Zeng et al, 2018 ; Dhyani et al, 2019 ). Therefore, the regulation of PPARα function has become one of the important strategies against cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

Salidroside Ameliorates Cardiomyocyte Hypertrophy by Upregulating Peroxisome Proliferator-Activated Receptor-α

et al. 2022

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Cardiac hypertrophy is an adaptive change in response to pressure overload, however the hypertrophy may evolve toward heart failure if cannot be corrected as soon as possible. The dysfunction of peroxisome proliferator-activated receptor-α (PPARα) plays a key role in cardiac hypertrophy. In the present study, salidroside inhibited the mRNA expressions of hypertrophic markers including atrial natriuretic factor and brain natriuretic peptide in a dosage-dependent manner. Furthermore, the protein expression and transcriptional activity of PPARα were increased by salidroside in H9C2 cells treated with angiotensin II, as well as the target genes of PPARα, while the situations were nearly reversed when PPARα was knocked down. Next, salidroside could elevate the expression of ATGL, a key upstream regulator of PPARα; the effects of salidroside including increasing PPARα function and inhibiting cardiomyocyte hypertrophy were impaired by ATGL knockdown. Our present studies suggested that salidroside elevated PPARα function to alleviate cardiomyocyte hypertrophy, which was involved in the increase of ATGL expression.

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“…An altered utilization of metabolic substrates is recognized as one of the biochemical hallmarks of the cardiac hypertrophy and failing heart ( Kumar et al, 2019 ). A number of studies indicated that cardiac energy metabolism occurred unavoidably in cardiac hypertrophy rat models induced by ISO or AAC ( Gao et al, 2015 ; Dhyani et al, 2019 ). CPT-1 mediates the uptake of long-chain fatty acids into mitochondria and plays an important role in the control and regulation of mitochondrial β-oxidation ( Jernberg et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

“…Although cardiac hypertrophy is known to occur due to oxidative stress, inflammation, and autophagy, the main cause has not been elucidated ( Li et al, 2016 ; Anthony et al, 2019 ; Geng et al, 2019 ). Recently, a number of studies report that metabolic dysfunction is a hallmark of cardiac hypertrophy and heart failure ( Tian et al, 2018 ; Dhyani et al, 2019 ). Previous findings in our laboratory and others have proved that the cardiac hypertrophy is also characterized by a metabolic switch in the utilization of energy source that uses glucose as an energy source rather than utilizing fatty acid ( Ingwall, 2009 ; Zou et al, 2013 ; Gao et al, 2015 ; Yue et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Bawei Chenxiang Wan Ameliorates Cardiac Hypertrophy by Activating AMPK/PPAR-α Signaling Pathway Improving Energy Metabolism

Zhang

Wang

et al. 2021

Front. Pharmacol.

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Bawei Chenxiang Wan (BCW), a well-known traditional Chinese Tibetan medicine formula, is effective for the treatment of acute and chronic cardiovascular diseases. In the present study, we investigated the effect of BCW in cardiac hypertrophy and underlying mechanisms. The dose of 0.2, 0.4, and 0.8 g/kg BCW treated cardiac hypertrophy in SD rat model induced by isoprenaline (ISO). Our results showed that BCW (0.4 g/kg) could repress cardiac hypertrophy, indicated by macro morphology, heart weight to body weight ratio (HW/BW), left ventricle heart weight to body weight ratio (LVW/BW), hypertrophy markers, heart function, pathological structure, cross-sectional area (CSA) of myocardial cells, and the myocardial enzymes. Furthermore, we declared the mechanism of BCW anti-hypertrophy effect was associated with activating adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferator–activated receptor-α (PPAR-α) signals, which regulate carnitine palmitoyltransferase1β (CPT-1β) and glucose transport-4 (GLUT-4) to ameliorate glycolipid metabolism. Moreover, BCW also elevated mitochondrial DNA-encoded genes of NADH dehydrogenase subunit 1(ND1), cytochrome b (Cytb), and mitochondrially encoded cytochrome coxidase I (mt-co1) expression, which was associated with mitochondria function and oxidative phosphorylation. Subsequently, knocking down AMPK by siRNA significantly can reverse the anti-hypertrophy effect of BCW indicated by hypertrophy markers and cell surface of cardiomyocytes. In conclusion, BCW prevents ISO-induced cardiomyocyte hypertrophy by activating AMPK/PPAR-α to alleviate the disturbance in energy metabolism. Therefore, BCW can be used as an alternative drug for the treatment of cardiac hypertrophy.

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Fenofibrate ameliorates neural, mechanical, chemical, and electrical alterations in the murine model of heart failure

Cited by 11 publications

References 36 publications

Energy metabolism disorders and potential therapeutic drugs in heart failure

Energy metabolism disorders and potential therapeutic drugs in heart failure

Salidroside Ameliorates Cardiomyocyte Hypertrophy by Upregulating Peroxisome Proliferator-Activated Receptor-α

Bawei Chenxiang Wan Ameliorates Cardiac Hypertrophy by Activating AMPK/PPAR-α Signaling Pathway Improving Energy Metabolism

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