Angiotensin II type 2 receptor mediates high fat diet-induced cardiomyocyte hypertrophy and hypercholesterolemia

Lima, Vanessa Batista de Sousa; Lino, Caroline Antunes; Senger, Nathalia; Silva, Tábatha de Oliveira; Fonseca, Roberto Cepêda; Bäder, Michael; Santos, Robson Augusto Souza; Júnior, José Donato; Barreto‐Chaves, Maria Luíza Morais; Diniz, Gabriela Placoná

doi:10.1016/j.mce.2019.110576

Cited by 6 publications

(3 citation statements)

References 51 publications

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“…This observation was further supported by an in vitro study showing that blocking AT 2 R with the antagonist PD123319 prevented leptin-induced cardiomyocyte hypertrophy. 121 This study is consistent with the finding that AT 2 R deletion protects against obesity.…”

Section: Organ Protectionsupporting

confidence: 92%

Angiotensin II Type 2 Receptor: A Target for Protection Against Hypertension, Metabolic Dysfunction, and Organ Remodeling

2021

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The renin-angiotensin system is of vital significance not only in the maintenance of blood pressure but also because of its role in the pathophysiology of different organ systems in the body. Of the 2 Ang II (angiotensin II) receptors, the AT 1 R (Ang II type 1 receptor) has been extensively studied for its role in mediating the classical functions of Ang II, including vasoconstriction, stimulation of renal tubular sodium reabsorption, hormonal secretion, cell proliferation, inflammation, and oxidative stress. The other receptor, AT 2 R (Ang II type 2 receptor), is abundantly expressed in both immune and nonimmune cells in fetal tissue. However, its expression is increased under pathological conditions in adult tissues. The role of AT 2 R in counteracting AT 1 R function has been discussed in the past 2 decades. However, with the discovery of the nonpeptide agonist C21, the significance of AT 2 R in various pathologies such as obesity, hypertension, and kidney diseases have been examined. This review focuses on the most recent findings on the beneficial effects of AT 2 R by summarizing both gene knockout studies as well as pharmacological studies, specifically highlighting its importance in blood pressure regulation, obesity/metabolism, organ protection, and relevance in the treatment of coronavirus disease 2019 (COVID-19).

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Section: Organ Protectionsupporting

confidence: 92%

Angiotensin II Type 2 Receptor: A Target for Protection Against Hypertension, Metabolic Dysfunction, and Organ Remodeling

2021

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“…30 Increases in ROS production stimulate cells to produce angiotensinogen then converted to angiotensin-2 (Ang-2) throughout the body. 8,[38][39][40] Furthermore, ROS can activate signaling kinases and transcription factors such as Rac GTP-binding protein, associated with fibrosis and hypertrophy, and the NF-κB pathway, related to pro-inflammatory gene transcription. 41 Moreover, visceral obesity is strongly correlated with epicardial adipose tissue, and it means a more significant amount of Ang-2 and pro-inflammatory adipokines production.…”

Section: Discussionmentioning

confidence: 99%

Improvement of Cardiac Fibrosis Biomarkers through Inflammation Inhibition by Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Administration in Metabolic Syndrome Rat Model

et al. 2021

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Background: Metabolic syndrome is a significant risk factor for cardiovascular diseases. Green tea and green coffee extracts, antioxidant and anti-inflammatory agents may participate in metabolic syndrome-induced cardiac fibrosis alleviation. However, the effect of combination of those extracts still needs exploration. Therefore, this study investigated the effect of green tea and decaffeinated light roasted green coffee extracts and their combination in metabolic syndrome-induced cardiac fibrosis rats. Methods: Metabolic syndrome rat model was i1nduced through high-fat high sucrose diets feeding for 8 weeks and injection of low dose streptozotocin at the 2nd week. The metabolic syndrome rats were divided into 4 experimental groups metabolic syndrome rats (MS); metabolic syndrome rats treated with 300 mg/ kg b.w green tea extract (GT); metabolic syndrome rats treated with 200 mg/ kg b.w decaffeinated light roasted green coffee extract (GC); metabolic syndrome rats treated with the combination of the two extracts (CE); and a normal control (NC) group was added. Angiotensin 2 level was analyzed by ELISA method. Gene expression of NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma were analyzed by touchdown polymerase chain reaction methods. Results: Metabolic syndrome rats treated with green tea and decaffeinated light roasted green coffee significantly decreased angiotensin-2 serum level and cardiac inflammation and fibrosis gene expression level (NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma). More significant alleviation was observed in the combination group. Conclusion: This study suggested that combination of green tea and decaffeinated light roasted green coffee extracts showed better improvement in metabolic syndrome-induced cardiac fibrosis rat model compared to that of single extract administration through inflammation inhibition

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“…Heart transverse sections were stained with picrosirius red to quantify the cardiac fibrosis area using Nikon (Tokyo, Japan) NIS Elements software ( n = 3–4 hearts per group). The fibrotic area was calculated as a relative area in relation to the total cardiac area, as previously described (Lima et al., 2019). Representative images were obtained using a microscope (Nikon, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

The miRNA‐143‐3p–Sox6–Myh7 pathway is altered in obesogenic diet‐induced cardiac hypertrophy

Silva

Lino

Miranda

et al. 2022

Experimental Physiology

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Obesity induces cardiometabolic disorders associated with a high risk of mortality. We have previously shown that the microRNA (miRNA) expression profile is changed in obesity-induced cardiac hypertrophy in male mice. Here, we investigated the effect of an obesogenic diet on the expression of miRNAs involved in cardiac hypertrophy in female mice. Female mice fed an obesogenic diet displayed an increased body weight gain, glucose intolerance, insulin resistance and dyslipidaemia. In addition, obese female mice exhibited cardiac hypertrophy associated with increased levels of several miRNAs, including miR-143-3p. Bioinformatic analysis identified Sox6, regulator of Myh7 gene transcription, as a predicted target of miR-143-3p. Female mice fed an obesogenic diet exhibited decreased mRNA levels of Sox6 and increased expression of Myh7 in the heart. Loss-of-function studies in cardiomyocytes revealed that inhibition of miR-143-3p increased Sox6 mRNA levels and reduced Myh7 expression. Collectively, our results indicate that obesity-associated cardiac hypertrophy in female mice is accompanied by alterations in diverse miRNAs, and suggest that the miR-143-3p-Sox6-Myh7 pathway may play a key role in obesity-induced cardiac hypertrophy.

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Angiotensin II type 2 receptor mediates high fat diet-induced cardiomyocyte hypertrophy and hypercholesterolemia

Cited by 6 publications

References 51 publications

Angiotensin II Type 2 Receptor: A Target for Protection Against Hypertension, Metabolic Dysfunction, and Organ Remodeling

Angiotensin II Type 2 Receptor: A Target for Protection Against Hypertension, Metabolic Dysfunction, and Organ Remodeling

Improvement of Cardiac Fibrosis Biomarkers through Inflammation Inhibition by Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Administration in Metabolic Syndrome Rat Model

The miRNA‐143‐3p–Sox6–Myh7 pathway is altered in obesogenic diet‐induced cardiac hypertrophy

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