The emerging role of ferroptosis in myocardial fibrosis of atrial fibrillation

Yue, Honghua; Zhan, Yujia; Zhang, Zheng; Liang, Weitao; Wu, Zhong

doi:10.5114/aoms/160941

Cited by 8 publications

(7 citation statements)

References 14 publications

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“…Ferroptosis is involved in myocardial fibrosis and several studies have investigated the relationship between ferroptosis and myocardial fibrosis. [ 17 ] Acot1 knockdown increases oxidative stress and inflammation and most likely results in fibrosis. [ 7 ] Researchers have proposed that LOX may play a role in a small proportion of cases of ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

KDM3A knockdown regulates COMP, LOX, COL8A1 and ACOT1 genes in myocardial fibrosis

Alzhrani,

Rasool,

Karim

et al. 2024

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Cardiovascular disease (CVD) is one of the main causes of death in Saudi Arabia. Cardiac remodeling plays a critical role in the pathophysiology of heart failure. Major focus of our study was to identify crucial genes involved in the pathological remodeling of the heart caused by pressure overload. We utilized various in-silico tools to analyze and interpret microarray data obtained from the Gene Expression Omnibus (GEO) database (GSE120739), including GEO2R analysis, Metascape analysis, WebGestalt analysis, and IPA (Ingenuity pathway analysis). Our findings indicate that certain genes, including Cartilage Oligomeric Matrix Protein (COMP), collagen type VIII alpha 1 chain (COL8A1) and Lysyl Oxidase (LOX) under the influence caused by knockdown of KDM3A, were down regulated by the extracellular matrix pathway. Moreover, genes, such as Acyl-CoA Thioesterase 1 (ACOT1) were up regulated by the fatty acid metabolism pathway. Overexpression of lysine-specific demethylase 3A (KDM3A) leads to the up regulation of fibrosis-related genes COMP, COL8A1, and LOX and the down regulation of ACOT1, result in enhanced fibrosis and heart failure. Our results suggest that COMP, COL8A1, LOX, and ACOT1 warrant further investigation in the development of cardiac fibrosis and as potential biomarkers for causing heart failure.

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Section: Discussionmentioning

confidence: 99%

KDM3A knockdown regulates COMP, LOX, COL8A1 and ACOT1 genes in myocardial fibrosis

Alzhrani,

Rasool,

Karim

et al. 2024

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“…However, the exploration of ferroptosis’s connection with AF remains relatively uncharted territory. At present, it has been shown that AF is associated with ferroptosis, including the bioactive molecules related to ferroptosis [ 36 ]. Therefore, a multi-dimensional analysis of ferroptosis in the context of AF is imperative.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study revealed a notable association between cardiomyocyte fibrosis and ferroptosis in patients with AF, with findings indicating a higher incidence of fibrosis in this group compared to controls [ 36 ]. The specific mechanisms linking atrial myocyte fibrosis and AF to ferroptosis, as well as the role of inflammation in this process, remain underexplored.…”

Section: The Role Of Ferroptosis and Inflammation In Afmentioning

confidence: 99%

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Focus on the Role of Inflammation as a Bridge between Ferroptosis and Atrial Fibrillation: A Narrative Review and Novel Perspective

Jin,

Zhong,

Gao

et al. 2024

Rev. Cardiovasc. Med.

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In this comprehensive review, we examine the intricate interplay between inflammation, ferroptosis, and atrial fibrillation (AF), highlighting their significant roles in AF pathophysiology and pathogenesis. Augmented inflammatory responses are pivotal to AF, potentially leading to atrial remodeling and reentry phenomena by impacting calcium channels and atrial tissue fibrosis. A strong correlation exists between inflammatory cytokines and AF, underscoring the importance of inflammatory signaling pathways, such as NOD-like receptor thermal protien domain associated protein 3 (NLRP3) inflammasome, Nuclear Factor kappa B (NF- B) signaling, and Tumor necrosis factor- (TNF- ) signaling in AF development. Ferroptosis, a non-apoptotic regulated mode of cell death, has been widely studied in relation to cardiovascular diseases including heart failure, myocardial infarction, cardiomyopathy, and reperfusion injury. The interaction between ferroptosis and inflammation is complex and mutually influential. While significant progress has been made in understanding the inflammation-AF relationship, the role of inflammation as a conduit linking ferroptosis and AF remains underexplored. The specific pathogenesis and key molecules of atrial fibrosis caused by ferroptosis are still not fully understood. Here we review the role of inflammatory signaling in ferroptosis and AF. We elucidated the association between ferroptosis and AF, aiming to unveil mechanisms for targeted inhibition of atrial cell fibrosis and to propose novel therapeutic strategies for AF. This exploration is vital for advancing our knowledge and developing more effective interventions for AF, a condition deeply intertwined with inflammatory processes and ferroptotic pathways.

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“…Yue et al . [ 27 ] analyzed samples of left ear tissue from patients suffering from persistent AF, and detected significantly higher iron particle levels in these samples via Prussian blue staining consistent with the AF-related dysregulation of iron metabolism. In line with these results, Rose et al .…”

Section: The Molecular and Metabolic Processes Between Ferroptosis An...mentioning

confidence: 96%

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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The emerging role of ferroptosis in myocardial fibrosis of atrial fibrillation

Cited by 8 publications

References 14 publications

KDM3A knockdown regulates COMP, LOX, COL8A1 and ACOT1 genes in myocardial fibrosis

KDM3A knockdown regulates COMP, LOX, COL8A1 and ACOT1 genes in myocardial fibrosis

Focus on the Role of Inflammation as a Bridge between Ferroptosis and Atrial Fibrillation: A Narrative Review and Novel Perspective

The Role of Ferroptosis in Atrial Fibrillation: A Promising Future

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