Trimedazidine alleviates pulmonary artery banding-induced acute right heart dysfunction and activates PRAS40 in rats

Cao, Yunshan; Song, Jiyang; Shen, Shutong; Fu, Heling; Li, Xiang; Xü, Ying; Wang, Aqian; Li, Xinli; Zhang, Min

doi:10.18632/oncotarget.20752

Cited by 4 publications

(7 citation statements)

References 61 publications

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“…Therefore, a rat model of PAB was adopted, because no pathological changes have been observed in the pulmonary parenchyma of this rat model and its phenotypes of acute RHF are predominantly, if not completely, caused by simple increase of afterload. 4 In the current study, also in the previous study, 10 we clipped the main pulmonary artery to induce a rapid increase in RV afterload and acute RHF. Afterwards, the high-throughput RNA-seq combined with bioinformatics analyses were employed to analyse gene expression profiling of the experimental groups.…”

Section: Discussionmentioning

confidence: 52%

“…The RV catheterization and PAB were performed as previously described. 10 Briefly, the rats were intubated with a 16-gauge Teflon tube and attached to a mechanical ventilator (Micro-Ventilator, UNO, Zevenaar, Netherlands) with the breathing frequency of 80 breaths / min, the pressures at 9/0 cmH 2 O, and the inspiratory/expiratory ratio of 1:1. The heads and limbs of the animals were fixed on an operating table.…”

Section: Methodsmentioning

confidence: 99%

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RNA‐sequencing analysis of gene expression in a rat model of acute right heart failure

Cao

et al. 2020

Pulm. circ.

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Background: Acute right heart failure (RHF) is the main cause of death in patients with acute pulmonary embolism and emergent pulmonary hypertension. However, the molecular mechanisms underpinning the acute RHF and the interactions between the right (RV) and left ventricles (LVs) under the diseased condition remain unknown. Methods and results: The Sprague Dawley male rats were randomly divided into the normal control, sham, and pulmonary artery banding (PAB) groups. One hour after the PAB operation, after measuring the haemodynamic and anatomical parameters, the free walls of RV and LV were harvested to detect the differential gene expression profiling by high-throughput RNA sequencing. The results showed that the PAB lead to 50–60% obstruction of the main pulmonary artery, which was accompanied by the significant elevation in the positive rate of rise in RV pressure and the maximum RV pressure as compared to the sham group. Moreover, compared with the counterparts in the sham group, the RV and LV in the PAB group exhibited 2057 differentially expressed genes (DEGs, 1159 upregulated and 898 downregulated) and 1196 DEGs (709 upregulated and 487 downregulated), respectively (DEG criteria: |log2 fold change| ≥1, q value ≤0.05). In comparison to the sham group, the enriched pathways in the PAB group include nuclear factor-κB signalling pathway, extracellular matrix–receptor interaction, and nucleotide oligomerization domain-like receptor signalling pathway. Conclusions: The PAB rat model exhibited the haemodynamic and gene expression changes in the RV that lead to acute RHF. Further, the acute RHF induced by pressure overload also caused gene expression changes in the LV, suggesting the molecular interactions between the RV and LV under the diseased condition.

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Section: Discussionmentioning

confidence: 52%

Section: Methodsmentioning

confidence: 99%

RNA‐sequencing analysis of gene expression in a rat model of acute right heart failure

Cao

et al. 2020

Pulm. circ.

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“…Models of transient pulmonary artery occlusion increase RV afterload by mechanical constriction of the pulmonary artery from the exterior or by inflation of intravascular balloons (48). External occlusion can be applied by ligature (43,44), snares (42), simple banding (40), or more advanced adjustable bands using air (41,45,46). The occlusion, and hence the PVR and RV strain, can be adjusted very precisely and, as opposed to PE models, the resistance can be reduced or even removed as the occlusion can be re-loosened.…”

Section: Models Of Transient Pulmonary Artery Occlusionmentioning

confidence: 99%

Animal models of right heart failure

Andersen¹,

Feen²,

Andersen³

et al. 2020

Cardiovasc Diagn Ther

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Right heart failure may be the ultimate cause of death in patients with acute or chronic pulmonary hypertension (PH). As PH is often secondary to other cardiovascular diseases, the treatment goal is to target the underlying disease. We do however know, that right heart failure is an independent risk factor, and therefore, treatments that improve right heart function may improve morbidity and mortality in patients with PH. There are no therapies that directly target and support the failing right heart and translation from therapies that improve left heart failure have been unsuccessful, with the exception of mineralocorticoid receptor antagonists. To understand the underlying pathophysiology of right heart failure and to aid in the development of new treatments we need solid animal models that mimic the pathophysiology of human disease. There are several available animal models of acute and chronic PH. They range from flow induced to pressure overload induced right heart failure and have been introduced in both small and large animals.When initiating new pre-clinical or basic research studies it is key to choose the right animal model to ensure successful translation to the clinical setting. Selecting the right animal model for the right study is hence important, but may be difficult due to the plethora of different models and local availability. In this review we provide an overview of the available animal models of acute and chronic right heart failure and discuss the strengths and limitations of the different models.

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“…Accumulating studies have suggested that the PGC-1α level is significantly decreased in various models of heart failure 81, 82. Additionally, activation of PGC-1β gene has been shown to also be reduced in response to chronic pressure overload, but is also dependent on, and responsive to, the chemical form of exogenous and dietary long chain fatty acids 6.…”

Section: The Role Of Pgc-1 In Heart Failurementioning

confidence: 99%

Blossoming 20: The Energetic Regulator's Birthday Unveils its Versatility in Cardiac Diseases

Lv¹,

Deng²,

Jiang³

et al. 2019

Theranostics

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The peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) was first identified in 1998 as a PGC-1 family member that regulates adaptive thermogenesis and mitochondrial function following cold exposure in brown adipose tissue. The PGC-1 family has drawn widespread attention over the past two decades as the energetic regulator. We recently summarized a review regarding PGC-1 signaling pathway and its mechanisms in cardiac metabolism. In this review, we elaborate upon the PGC-1 signaling network and highlight the recent progress of its versatile roles in cardiac diseases, including myocardial hypertrophy, peripartum and diabetic cardiomyopathy, and heart failure. The information reviewed here may be useful in future studies, which may increase the potential of this energetic regulator as a therapeutic target.

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Trimedazidine alleviates pulmonary artery banding-induced acute right heart dysfunction and activates PRAS40 in rats

Cited by 4 publications

References 61 publications

RNA‐sequencing analysis of gene expression in a rat model of acute right heart failure

RNA‐sequencing analysis of gene expression in a rat model of acute right heart failure

Animal models of right heart failure

Blossoming 20: The Energetic Regulator's Birthday Unveils its Versatility in Cardiac Diseases

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