Melatonin inhibits angiotensin II–induced atrial fibrillation through preventing degradation of Ang II Type I Receptor–Associated Protein (ATRAP)

Xie, Xin; Shen, Tingting; Bi, Hai-Lian; Su, Zhuo-Lin; Liao, Zi-Qi; Zhang, Ying; Shi, Lei

doi:10.1016/j.bcp.2022.115146

Cited by 4 publications

(1 citation statement)

References 41 publications

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“…Mice were anesthetized by administration of 2.5% tribromoethanol (0.02 mL/g; Sigma-Aldrich, St. Louis, MO, USA), then a Millar 1.1F octapolar EP catheter (Scisense) was inserted into the right atrium via the right jugular vein, as others previously described 20 . The stimulation voltages were delivered at a voltage magnitude 3.5v, 5v, and 8v, and the frequencies were decreased from 40Hz to 20Hz at a frequency space of 2Hz.…”

Section: Af Stimulationmentioning

confidence: 99%

ATG5 gene delivery by rAAV9 promotes doxorubicin-induced atrial fibrillation and structural remodeling

Xie,

Li,

Wang

et al. 2024

Preprint

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Doxorubicin (DOX) is used as first-line chemotherapeutic drug in treating various cancers. However, patients with DOX administration are susceptible to atrial fibrillation (AF) with unknown mechanisms. Numerous previous studies have shown that autophagy plays an important role in the development of AF, but autophagy protein 5 (ATG5) in DOX-induced AF has still not been studied. Mice were intraperitoneally injected with DOX (5mg/kg) for 4 weeks to establish AF model. AF was documented by telemetry in vivo, the atria were assessed for molecular biological and morphological analyses. HL-1 cells were treated with DOX, then autophagy flux and oxidative stress were detected by confocal microscopy and DCF-DA staining. Here, we found that autophagy related genes including ATG5, Beclin-1, ATG12 and LC3B were upregulated in DOX-treated HL-1 cells. DOX treatment resulted in AF, atrial fibrosis and oxidative stress in mice, which were mitigated by rAAV9 expressing shRNA-ATG5 and aggravated by rAAV9 expressing ATG5. In addition, DOX treatment increased autophagosome but blocked autophagic flux, increased ROS generation and induced oxidative stress in HL-1 cells. These effects were markedly attenuated by siRNA-ATG5, whereas aggravated by adenovirus expressing ATG5 in HL-1 cells. Mechanically, we found DOX caused AF through ATG5-mediated autophagy which further regulated oxidative stress and atrial fibrosis. Overall, our study demonstrated that ATG5-mediated autophagy aggravated DOX–induced AF.

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Section: Af Stimulationmentioning

confidence: 99%