Mitochondrial Dysfunction in Atrial Tissue of Patients Developing Postoperative Atrial Fibrillation

Jeganathan, Jelliffe; Saraf, Rabya; Mahmood, Feroze; Pal, Anam; Bhasin, Manoj; Huang, Ting-Yi; Mittel, Aaron; Knio, Ziyad O.; Simons, Russell; Khabbaz, Kamal R.; Senthilnathan, Venkatachalam; Liu, David; Sellke, Frank W.; Matyal, Robina

doi:10.1016/j.athoracsur.2017.04.060

Cited by 34 publications

(31 citation statements)

References 16 publications

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“…In research similar to the current study, using the measurement method from dried blood, Zhansheng et al partially showed that carnitine and esters could be used in the differentiation of haemorrhagic and ischaemic stroke [34]. In another study, Jeganathan et al reported that mitochondrial dysfunction could play a role in postoperative atrial fibrillation [35].…”

Section: Discussionsupporting

confidence: 70%

Rapid and sensitive determination of carnitine profiling by tandem mass spectrometry can be a diagnostic marker of paroxysmal atrial fibrillation

Koyuncu¹

2018

Ann Clin Anal Med

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Aim: Paroxysmal atrial fibrillation (PAF), which is in the sub-group of atrial fibrillation that spontaneously resolves within 48 hours and does not last more than 7 days, is one of the most important causes of cryptogenic stroke. Other than ECG findings, there are no biochemical diagnostic criteria for PAF. Early diagnosis of PAF reduces the risk of morbidity and mortality. Therefore, it is important to identify new diagnostic markers. Metabolomics methods have recently started to be used for this purpose. Carnitine profiling with LC-MS/MS is a fast, inexpensive metabolomics screening method with high sensitivity and has started to be used for the determination of new diagnostic markers. The aim of this study was to investigate the viability of the carnitine profile as a new biochemical marker supporting diagnosis in PAF patients. Material and Method: A total of 27 carnitine ester profiles were examined with the LC-MS/MS method using serum samples taken from 41 patients diagnosed with PAF from ECG findings and 42 healthy individuals with sinus rhythm. Results: The C14, C16:1, and C18:1 serum carnitine ester levels of the PAF patients were determined to be statistically significantly higher than those of the healthy control group (p<0.05) and C6DC levels were found to be significantly lower (p<0.05). Discussion: The results of the study strengthened the view that with measurements made with LC-

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Section: Discussionsupporting

confidence: 70%

Rapid and sensitive determination of carnitine profiling by tandem mass spectrometry can be a diagnostic marker of paroxysmal atrial fibrillation

Koyuncu¹

2018

Ann Clin Anal Med

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“…Indeed, abnormal mitochondrial structure and function have been reported in animal model of AF [26], Moreover, the atria of non-diabetic patients with AF already display enhanced mitochondrial DNA damage [27,28], and reduced respiratory capacity [27,29]. Mitochondrial dynamics are also altered in patients with AF, characterized by a reduction in mitochondrial biogenesis [30]. Specifically, Jeganathan et al observed that the main regulator of mitochondrial biogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is downregulated in atrial tissue from patients with post-operative AF [30].…”

Section: Mitochondrial Dysfunction In T2dm and Afmentioning

confidence: 99%

“…Mitochondrial dynamics are also altered in patients with AF, characterized by a reduction in mitochondrial biogenesis [30]. Specifically, Jeganathan et al observed that the main regulator of mitochondrial biogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is downregulated in atrial tissue from patients with post-operative AF [30]. Furthermore, molecular markers for mitochondrial volume are also reduced in the atrial tissue from patients with AF [31].…”

Section: Mitochondrial Dysfunction In T2dm and Afmentioning

confidence: 99%

Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?

Yurista

Silljé

Rienstra

et al. 2020

Cardiovasc Diabetol

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While patients with type 2 diabetes mellitus (T2DM) are at increased risk to develop atrial fibrillation (AF), the mechanistic link between T2DM and AF-susceptibility remains unclear. Common co-morbidities of T2DM, particularly hypertension, may drive AF in the setting of T2DM. But direct mechanisms may also explain this relation, at least in part. In this regard, recent evidence suggests that mitochondrial dysfunction drives structural, electrical and contractile remodelling of atrial tissue in patients T2DM. Mitochondrial dysfunction may therefore be the mechanistic link between T2DM and AF and could also serve as a therapeutic target. An elegant series of experiments published in Cardiovascular Diabetology provide compelling new evidence to support this hypothesis. Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF. But the authors also demonstrated that the sodium-glucose co-transporter 2 inhibitors (SGLT2i) empagliflozin has the capacity to restore mitochondrial function, ameliorate electrical and structural remodelling and prevent AF. These findings provide a new horizon in which mitochondrial targeted therapies could serve as a new class of antiarrhythmic drugs.

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“…These remodeling approaches include structural remodeling characterized as atrial fibrosis (Frustaci et al, 1997) and atrial adipose (Hatem and Sanders, 2014), electrical remodeling featured by changes in ion channels and gap junction proteins (Lai et al, 1999), and endocardial and metabolic remodeling (Schild et al, 2006;Jeganathan et al, 2017). Numerous basic studies have been conducted to explore the roles of electric, structural and contractile remodeling in the pathophysiological changes of AF.…”

Section: Introductionmentioning

confidence: 99%

Proteomic Analysis of Atrial Appendages Revealed the Pathophysiological Changes of Atrial Fibrillation

Liu

Zhao

et al. 2020

Front. Physiol.

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Atrial fibrillation (AF), known as the most common arrhythmia in the developed world, affects 1.5-2.0% of the population. Numerous basic studies have been carried out to identify the roles of electric and structural remodeling in the pathophysiological changes of AF, but more explorations are required to further understand the mechanisms of AF development. Proteomics enables researchers to identify protein alterations responsible for the pathological developing progresses of diseases. Compared to the genome, the proteome is closely related to the disease phenotype and can better manifest the progression of diseases. In this study, AF patients proteomically analyzed to identify possible mechanisms. Totally 20 patients undergoing cardiac surgery (10 with paroxysmal AF and 10 with persistent AF) and 10 healthy subjects were recruited. The differentially expressed proteins identified here included AKR1A1,

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Mitochondrial Dysfunction in Atrial Tissue of Patients Developing Postoperative Atrial Fibrillation

Abstract: Compared with patients without POAF, those with POAF demonstrated mitochondrial dysfunction at various levels that are suitable for potential pharmacotherapy.

Cited by 34 publications

References 16 publications

Rapid and sensitive determination of carnitine profiling by tandem mass spectrometry can be a diagnostic marker of paroxysmal atrial fibrillation

Rapid and sensitive determination of carnitine profiling by tandem mass spectrometry can be a diagnostic marker of paroxysmal atrial fibrillation

Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?

Proteomic Analysis of Atrial Appendages Revealed the Pathophysiological Changes of Atrial Fibrillation

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