Chronic catestatin treatment reduces atrial fibrillation susceptibility via improving calcium handling in post-infarction heart failure rats

Yan, Min; Liu, Tao; Zhong, Peng; Xiong, Feng; Cui, Bo; Wu, Jinchun; Wu, Gang

doi:10.1016/j.peptides.2022.170904

Cited by 4 publications

(4 citation statements)

References 54 publications

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“…In canine PVs, sympathetic activation induced an increase in myocardial cytoplasmatic (Ca 2+ ), which was required for early afterdepolarizations in PVs and consequently triggered AF [ 36 ]. In vitro studies have shown that chronic catestatin treatment reduces AF vulnerability in rats with myocardial infarction (MI)-induced HF by improving Ca 2+ handling through preserved SR Ca 2+ -ATPase protein expression but reducing the protein levels of phosphorylated-ryanodine receptor two and phosphorylated-Ca 2+ /calmodulin-dependent protein kinase II in the atria [ 37 ]. Exogenous catestatin enhanced autonomic function, decreased QT interval and action potential duration, and reduced experimentally induced ventricular arrhythmias in a rat model of myocardial infarction [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Serum Catestatin Concentrations Are Increased in Patients with Atrial Fibrillation

Katić

Jurišić

Kumrić

et al. 2023

JCDD

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The autonomic nervous system is crucial in initiating and maintaining atrial fibrillation (AF). Catestatin is a multipurpose peptide that regulates cardiovascular systems and reduces harmful, excessive activity of the sympathetic nervous system by blocking the release of catecholamines. We aimed to determine whether serum catestatin concentrations are associated with AF severity, duration indices, and various clinical and laboratory indicators in these individuals to better define the clinical value of catestatin in patients with AF. The present single center study enrolled 73 participants with AF and 72 healthy age-matched controls. Serum catestatin concentrations were markedly higher in AF patients than controls (14.11 (10.21–26.02) ng/mL vs. 10.93 (5.70–20.01) ng/mL, p = 0.013). Furthermore, patients with a more severe form of AF had significantly higher serum catestatin (17.56 (12.80–40.35) vs. 10.98 (8.38–20.91) ng/mL, p = 0.001). Patients with higher CHA2DS2-VASc scores (17.58 (11.89–37.87) vs. 13.02 (8.47–22.75) ng/mL, p = 0.034) and higher NT-proBNP levels (17.58 (IQR 13.91–34.62) vs. 13.23 (IQR 9.04–22.61), p = 0.036) had significantly higher serum catestatin concentrations. Finally, AF duration correlated negatively with serum catestatin levels (r = −0.348, p = 0.003). The results of the present study implicate the promising role of catestatin in the intricate pathophysiology of AF, which should be explored in future research.

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Section: Discussionmentioning

confidence: 99%

Serum Catestatin Concentrations Are Increased in Patients with Atrial Fibrillation

Katić

Jurišić

Kumrić

et al. 2023

JCDD

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“…CaTs were recorded in LVCMs with 1 Hz electrically field stimulation at 37°C. As previously described, 13,20 the amplitude of CaT, the diastolic [Ca 2+ ] i level, as well as CaT decay time constant were measured to evaluate cellular Ca 2+ handling. Additionally, the sarcoplasmic reticulum (SR) Ca 2+ content ([Ca 2+ ] SR ) was measured by rapidly adding caffeine (10 mm) after a train of 1 Hz electrically field stimulation.…”

Section: Methodsmentioning

confidence: 99%

Dapagliflozin attenuates cardiac remodeling and dysfunction in rats with β-adrenergic receptor overactivation through restoring calcium handling and suppressing cardiomyocyte apoptosis

Liu,

Wu,

Shi

et al. 2023

Diabetes and Vascular Disease Research

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Background: Long-term β-adrenergic receptor (β-AR) activation can impair myocardial structure and function. Dapagliflozin (DAPA) has been reported to improve clinical prognosis in heart failure patients, whereas the exact mechanism remains unclear. Here, we investigated the effects of DAPA against β-AR overactivation toxicity and explored the underlying mechanism. Methods and Results: Rats were randomized to receive saline + placebo, isoproterenol (ISO, 5 mg/kg/day, intraperitoneally) + placebo, or ISO + DAPA (1 mg/kg/day, intragastrically) for 2-week. DAPA treatment improved cardiac function, alleviated myocardial fibrosis, prevented cardiomyocytes (CMs) apoptosis, and decreased the expression of ER stress-mediated apoptosis markers in ISO-treated hearts. In isolated CMs, 2-week ISO stimulation resulted in deteriorated kinetics of cellular contraction and relaxation, increased diastolic intracellular Ca2+ level and decay time constant of Ca2+ transient (CaT) but decreased CaT amplitude and sarcoplasmic reticulum (SR) Ca2+ level. However, DAPA treatment prevented abnormal Ca2+ handling and contractile dysfunction in CMs from ISO-treated hearts. Consistently, DAPA treatment upregulated the expression of SR Ca2+-ATPase protein and ryanodine receptor 2 (RyR2) but reduced the expression of phosphorylated-RyR2, Ca2+/calmodulin-dependent protein kinase II (CaMKII), and phosphorylated-CaMKII in ventricles from ISO-treated rats. Conclusion: DAPA prevented myocardial remodeling and cardiac dysfunction in rats with β-AR overactivation via restoring calcium handling and suppressing ER stress-related CMs apoptosis.

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“…16 Increased diastolic sarcoplasmic reticulum (SR) Ca 2+ leakage and decreased SR Ca 2+ reuptake due to sarcoplasmic reticulum Ca 2+ -ATPase (SERCA2a) downregulation which leads to elevated intracellular Ca 2+ level ([Ca 2+ ] i ) in atrial myocytes. 17 It has been shown that elevated [Ca 2+ ] i promotes Na + influx by activating the Na + -Ca 2+ exchanger (NCX) to provide delayed afterdepolarizations (DADS), which is a significant cause of triggered activity to initiate AF. 18 Among them, ryanodine receptor 2 (RyR2) is the key target and other proteins regulating RyR2 also play an irreplaceable role in the pathophysiological process.…”

Section: Calcium Handling Ion Channels Iron Disturbancementioning

confidence: 99%

“…Numerous studies have demonstrated that abnormal calcium handling holds a crucial part in the initiation and maintenance of AF via favor the genesis of triggered activity in the atria, which is the primary mechanism responsible for AF 16 . Increased diastolic sarcoplasmic reticulum (SR) Ca 2+ leakage and decreased SR Ca 2+ reuptake due to sarcoplasmic reticulum Ca 2+ ‐ATPase (SERCA2a) downregulation which leads to elevated intracellular Ca 2+ level ([Ca 2+ ] i ) in atrial myocytes 17 . It has been shown that elevated [Ca 2+ ] i promotes Na + influx by activating the Na + ‐Ca 2+ exchanger (NCX) to provide delayed afterdepolarizations (DADS), which is a significant cause of triggered activity to initiate AF 18 .…”

Section: Calcium Handling Ion Channels Iron Disturbancementioning

confidence: 99%

Iron and atrial fibrillation: A review

Liu

Yang

et al. 2023

Pacing Clinical Electrophis

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Atrial fibrillation (AF), one of the most common arrhythmias in clinical practice, is classified into paroxysmal, persistent, and permanent AF according to its duration. The development of AF is associated with increased cardiovascular morbidity and mortality. However, the exact etiology of this disease remains poorly understood. Recent studies found disorders of iron metabolism might be involved in the progression of AF. Abnormal iron metabolism in cardiomyocytes provides arrhythmogenic substrates through a variety of mechanisms, including calcium mishandling, ion channel remodeling, and oxidative stress overaction. Interestingly, in AF patients with iron overload, interventions on iron metabolism, such as iron chelators and ferroptosis inhibitors, has been shown to prevent AF via reducing ferroptosis. Herein, we review the possible mechanisms, consequences, and therapeutic implications of altered atrial iron handling for AF pathophysiology.

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Chronic catestatin treatment reduces atrial fibrillation susceptibility via improving calcium handling in post-infarction heart failure rats

Cited by 4 publications

References 54 publications

Serum Catestatin Concentrations Are Increased in Patients with Atrial Fibrillation

Serum Catestatin Concentrations Are Increased in Patients with Atrial Fibrillation

Dapagliflozin attenuates cardiac remodeling and dysfunction in rats with β-adrenergic receptor overactivation through restoring calcium handling and suppressing cardiomyocyte apoptosis

Iron and atrial fibrillation: A review

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