Invasive therapies for patients with concomitant heart failure and atrial fibrillation

Wei, Wei; Shehata, Michael; Wang, Xunzhang; Rao, Fang; Xian-zhan, Zhan; Guo, Huiming; Fang, Xianhong; Liao, Hongtao; Liu, Jian; Deng, Hai; Liu, Yang; Xue, Yan; Wu, Shulin

doi:10.1007/s10741-019-09795-0

Cited by 4 publications

(3 citation statements)

References 76 publications

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“…Atrial fibrillation is a prevalent and severe arrhythmia disease worldwide, often leading to recurrent episodes and, in some cases, permanent AF that can induce cardiac insufficiency [ 16 ]. This study aimed to explore new drugs for preventing and treating AF.…”

Section: Discussionmentioning

confidence: 99%

Neferine mitigates angiotensin II-induced atrial fibrillation and fibrosis via upregulation of Nrf2/HO-1 and inhibition of TGF-β/p-Smad2/3 pathways

Jiang,

Zhang,

Wang

2024

Aging

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Background: Atrial fibrillation (AF) is often associated with atrial fibrosis and oxidative stress. Neferine, a bisbenzylisoquinoline alkaloid, has been reported to exert an antiarrhythmic effect. However, its impact on Angiotensin II (Ang II) infusion-induced AF and the underlying mechanism remains unclear. This study aimed to investigate whether neferine alleviates Ang II-induced AF and explore the underlying mechanisms. Methods: Mice subjected to Ang II infusion to induce AF were concurrently treated with neferine or saline. AF incidence, myocardial cell size, fibrosis, and oxidative stress were then examined. Results: Neferine treatment inhibited Ang II-induced AF, atrial size augmentation, and atrial fibrosis. Additionally, we observed that Ang II increased reactive oxygen species (ROS) generation, induced mitochondrial membrane potential depolarization, and reduced glutathione (GSH) and superoxide dismutase (SOD) levels, which were reversed to some extent by neferine. Mechanistically, neferine activated the Nrf2/HO-1 signaling pathway and inhibited TGF-β/p-Smad2/3 in Ang II-infused atria. Zinc Protoporphyrin (ZnPP), an HO-1 inhibitor, reduced the anti-oxidative effect of neferine to some extent and subsequently abolished the beneficial effect of neferine on Ang II-induced AF. Conclusions: These findings provide hitherto undocumented evidence that the protective role of neferine in Ang II-induced AF is dependent on HO-1.

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Section: Discussionmentioning

confidence: 99%

Neferine mitigates angiotensin II-induced atrial fibrillation and fibrosis via upregulation of Nrf2/HO-1 and inhibition of TGF-β/p-Smad2/3 pathways

Jiang,

Zhang,

Wang

2024

Aging

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“…Atrial fibrillation (AF) represents a highly prevalent arrhythmia [ 1 ]. Most of the patients with AF are prone to recurrent attacks after rhythmic transformation, which may lead to permanent AF and hence induce cardiac insufficiency as well as embolic diseases [ 23 , 24 ]. Therefore, there is urgent need to explore pathogenesis of AF and develop new therapies to prevent and treat AF.…”

Section: Discussionmentioning

confidence: 99%

Exosomes from Bone Marrow Mesenchymal Stem Cells with Overexpressed Nrf2 Inhibit Cardiac Fibrosis in Rats with Atrial Fibrillation

Fan

et al. 2022

Cardiovascular Therapeutics

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Background. Even though nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling has been associated with the pathogenesis of multiple heart conditions, data on roles of Nrf2 within atrial fibrillation (AF) still remain scant. The present investigation had the aim of analyzing Nrf2-overexpressing role/s upon bone mesenchymal stem cell- (BMSC-) derived exosomes in rats with AF. Methods. Exosomes were collected from control or Nrf2 lentivirus-transduced BMSCs and then injected into rats with AF through the tail vein. AF duration was observed using electrocardiography. Immunohistochemical staining was then employed for assessing Nrf2, HO-1, α-SMA, collagen I, or TGF-β1 expression profiles within atrial myocardium tissues. Conversely, Masson staining was utilized to evaluate atrial fibrosis whereas apoptosis within myocardia was evaluated through TUNEL assays. In addition, TNF-α, IL-1β, IL-4, or IL-10 serum expression was assessed through ELISA. Results. Results of the current study showed significant downregulation of Nrf2/HO-1 within AF rat myocardia. It was found that injection of the control or Lv-Nrf2 exosomes significantly alleviated and lowered AF timespans together with reducing cardiomyocyte apoptosis. Moreover, injection of Lv-Nrf2 exosomes essentially lowered AF-driven atrial fibrosis and also inhibited inflammatory responses in the rats with AF. Conclusion. Delivery of BMSC-derived exosomes using overexpressed Nrf2 inhibited AF-induced arrhythmias, myocardial fibrosis, apoptosis, and inflammation via Nrf2/HO-1 pathway triggering.

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“…Approximately 33 million individuals throughout the globe are impacted by AF, and this number is forecast to double over the next four decades [ 2 ]. AF is typically related to a variety of other forms of cardiovascular diseases such as hypertension, cardiomyopathy, and coronary artery disease, potentially contributing to heart failure, stroke, thromboembolism, and potential death [ 3 ]. AF is a multifactorial and highly complex disease such that its precise pathological basis remains elusive, although structural and electrical remodeling, abnormal calcium homeostasis, and dysfunction of the autonomic nervous system are thought to contribute [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

The Role of Ferroptosis in Atrial Fibrillation: A Promising Future

Zhou,

Qian,

et al. 2024

Rev. Cardiovasc. Med.

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Atrial fibrillation (AF) is one of the most common cardiac arrhythmias, with its diagnosis being closely tied to higher rates of cardiovascular morbidity and mortality. AF is associated with a range of dangerous complications including stroke and heart failure, making it a key driver of healthcare spending and a major threat to global public health. The precise mechanisms that govern AF incidence and the onset of related complications, however, remain uncertain. Ferroptotic cell death has been the focus of rising interest in the cardiac arrhythmias, and there is recent evidence supporting a role for atrial ferroptosis as a mediator of AF development. Interventional strategies focused on ferroptotic activity, such as novel ferroptosis inhibitors, have also shown promise as a means of protecting against AF through their ability to reduce iron overload. In this review, we provide a summary of the proposed mechanisms whereby ferroptosis contributes to the pathophysiology of AF and their therapeutic implications.

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Invasive therapies for patients with concomitant heart failure and atrial fibrillation

Cited by 4 publications

References 76 publications

Neferine mitigates angiotensin II-induced atrial fibrillation and fibrosis via upregulation of Nrf2/HO-1 and inhibition of TGF-β/p-Smad2/3 pathways

Neferine mitigates angiotensin II-induced atrial fibrillation and fibrosis via upregulation of Nrf2/HO-1 and inhibition of TGF-β/p-Smad2/3 pathways

Exosomes from Bone Marrow Mesenchymal Stem Cells with Overexpressed Nrf2 Inhibit Cardiac Fibrosis in Rats with Atrial Fibrillation

The Role of Ferroptosis in Atrial Fibrillation: A Promising Future

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