Iron and atrial fibrillation: A review

Ju, Hehua; Liu, Tao; Yang, Manqi; Cheng, Mian; Wu, Gang

doi:10.1111/pace.14678

Cited by 4 publications

(5 citation statements)

References 80 publications

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“…Several studies have discovered that a loss-of-function mutation in GATA5 is associated with AF, (11).…”

Section: Discussionmentioning

confidence: 99%

“…Severe cognitive disability, stereotypic movements, epilepsy and cerebral malformation have been linked to mutations and deletions at this locus (30). It's reported that in AF patients with iron overload, interventions in iron metabolism, such as iron chelators and iron removal inhibitors, have been shown to prevent AF by reducing iron mortality (11).…”

Section: Discussionmentioning

confidence: 99%

“…Hitherto, it's reported that ferroptosis was involved in several cardiovascular diseases, such as myocardial infarction, diabetic cardiomyopathy and signi cantly AF (10). In addition, recent studies showed the promoting role of ferroptosis in the development of AF (11). A growing number of evidences recognized that iron-overload brought about AF pathophysiology and Nomani et al found that cardiac ferric iron overload and the iron-dependent oxidative stress were the major cause of AF in β-thalassemia patients (5,12).…”

Section: Introductionmentioning

confidence: 99%

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Identification of potential Ferroptosis-Related Biomarkers and Immune Infiltration in Human Atrial Fibrillation

Wang,

Yang,

Xiong

et al. 2024

Preprint

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Background The role of structural remodeling in the development and persistence of atrial fibrillation atrial fibrillation (AF) is significant, although its mechanism remains unknown at present. This study aims to explore the transcriptomic mechanisms of AF structural remodeling through bioinformatics analysis. Methods These microarrays GSE14975, GSE31821 and GSE79768 were acquired from the GEO database. Next, a series of bioinformatics methods were used, such as R language, DAVID, STING, and Cytoscape software, to study the DEG between AF and control samples. Then, we found genes related to ferroptosis from FerrDb database and conducted joint analysis with differentially expressed genes (DEG). In addition, we predicted several transcription factors that regulate DEG and conducted immune infiltration analysis using CIBERSORT software. Results a total of 363 up-regulated DEGs and 308 down-regulated DEGs were identified from atrium cordis samples of 16 AF patients and 13 controls. Functional changes of DEGs mainly focus on positive regulation of inflammatory response, signal transduction, inflammatory response, immune response, oxidation-reduction process and extracellular matrix organization. Eleven DE-FRGs were identified, including HSPB1, ALOX15, ETV4, ACO1, CHAC1, FH, PARP15, IFNG, ACSL1, FABP4 and IL1B and several TFs (POLE2, GATA5, CEBPA, ATF3, MEF2C) were predicted via Cytoscape software. Macrophage M2 was found to occupy the largest proportion of all the immune cells. Conclusion The occurrence of AF may be a result of fibrosis caused by myocardial cell ferroptosis and imbalance of the immune microenvironment. Obtained DE-FRGs HSPB1, ALOX15, ETV4, ACO1, CHAC1, FH, PARP15, IFNG, ACSL1, FABP4 and IL1B and predicted TFs POLE2, GATA5, CEBPA, ATF3, MEF2C can be seen as potential targets for preventing AF.

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“…Several studies have discovered that a loss-of-function mutation in GATA5 is associated with AF, (11).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of potential Ferroptosis-Related Biomarkers and Immune Infiltration in Human Atrial Fibrillation

Wang,

Yang,

Xiong

et al. 2024

Preprint

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“…Iron deposition in the heart’s atria can have a significant impact on the occurrence and development of supraventricular arrhythmias. Abnormal iron levels can lead to dysregulation of calcium handling, affecting the normal electrical signals, and to changes in the expression and function of ion channels, which regulate the heart’s electrical activity, and promote oxidative stress, creating the electrical and structural remodeling that predisposes to supraventricular arrhythmias [ 51 ]. It has been proven that increased levels of reactive oxygen species (ROS) are associated with atrial fibrillation through changes in both local (atrial cardiomyocytes) and systemic (serum) activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), an enzyme complex that generates ROS [ 52 , 53 , 54 ].…”

Section: Discussionmentioning

confidence: 99%

Pancreatic T2* Magnetic Resonance Imaging for Prediction of Cardiac Arrhythmias in Transfusion-Dependent Thalassemia

Meloni,

Pistoia,

Ricchi

et al. 2023

JCM

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We assessed the value of pancreatic T2* magnetic resonance imaging (MRI) for predicting cardiac events from a large prospective database of transfusion-dependent thalassemia (TDT) patients. We considered 813 TDT patients (36.47 ± 10.71 years, 54.6% females) enrolled in the Extension-Myocardial Iron Overload in Thalassemia Network. MRI was used to measure hepatic, pancreatic, and cardiac iron overload (IO), to assess biventricular function and atrial dimensions, and to detect replacement myocardial fibrosis. The mean follow-up was 50.51 ± 19.75 months. Cardiac complications were recorded in 21 (2.6%) patients: one with heart failure (HF) and 20 with arrhythmias. The single patient who developed HF had, at the baseline MRI, a reduced pancreas T2*. Out of the 20 recorded arrhythmias, 17 were supraventricular. Pancreatic T2* values were a significant predictor of future arrhythmia-related events (hazard ratio = 0.89; p = 0.015). Pancreas T2* remained significantly associated with future arrhythmias after adjusting for any other univariate predictor (age and male sex, diabetes, history of previous arrhythmias, or left atrial area index). According to the receiver-operating characteristic curve analysis for arrhythmias, a pancreas T2* < 6.73 ms was the optimal cut-off value. In TDT, pancreatic iron levels had significant prognostic power for arrhythmias. Regular monitoring and the development of targeted interventions to manage pancreatic IO may help improve patient outcomes.

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“…Furthermore, TNF-

may also promote AF by acting on gap links such as connexin 40,43 (CX40, CX43) [ 86 , 87 ]. One review concluded that TNF-

, as one of the hallmark inflammatory pathways of inflammation and oxidative stress in ferroptosis, may interfere with CX40 and CX43 in the atrial gap [ 88 ]. In addition, pinocembrin has also been found to regulate the expression of CX40 and other ion channels in cardiomyocytes by inhibiting inflammation [ 89 ].…”

Section: The Role Of Ferroptosis and Inflammation In Afmentioning

confidence: 99%

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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Iron and atrial fibrillation: A review

Cited by 4 publications

References 80 publications

Identification of potential Ferroptosis-Related Biomarkers and Immune Infiltration in Human Atrial Fibrillation

Identification of potential Ferroptosis-Related Biomarkers and Immune Infiltration in Human Atrial Fibrillation

Pancreatic T2* Magnetic Resonance Imaging for Prediction of Cardiac Arrhythmias in Transfusion-Dependent Thalassemia

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

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