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Arzt, Michael; Drzymalski, Marzena A.; Ripfel, Sarah; Meindl, Sebastian; Biedermann, Alexander; Durczok, Melanie; Keller, Karoline; Mustroph, Julian; Katz, Sylvia; Tafelmeier, Maria; Lebek, Simon; Flörchinger, Bernhard; Camboni, Daniele; Wittmann, Sigrid; Backs, Johannes; Schmid, Christof; Maier, Lars S.; Wagner, Stefan

Enhanced Cardiac CaMKII Oxidation and CaMKII-Dependent SR Ca Leak in Patients with Sleep-Disordered Breathing

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  • Medientyp: E-Artikel
  • Titel: Enhanced Cardiac CaMKII Oxidation and CaMKII-Dependent SR Ca Leak in Patients with Sleep-Disordered Breathing
  • Beteiligte: Arzt, Michael; Drzymalski, Marzena A.; Ripfel, Sarah; Meindl, Sebastian; Biedermann, Alexander; Durczok, Melanie; Keller, Karoline; Mustroph, Julian; Katz, Sylvia; Tafelmeier, Maria; Lebek, Simon; Flörchinger, Bernhard; Camboni, Daniele; Wittmann, Sigrid; Backs, Johannes; Schmid, Christof; Maier, Lars S.; Wagner, Stefan
  • Erschienen: MDPI AG, 2022
  • Erschienen in: Antioxidants
  • Sprache: Englisch
  • DOI: 10.3390/antiox11020331
  • ISSN: 2076-3921
  • Schlagwörter: Cell Biology ; Clinical Biochemistry ; Molecular Biology ; Biochemistry ; Physiology
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:p>Background: Sleep-disordered breathing (SDB) is associated with increased oxidant generation. Oxidized Ca/calmodulin kinase II (CaMKII) can contribute to atrial arrhythmias by the stimulation of sarcoplasmic reticulum Ca release events, i.e., Ca sparks. Methods: We prospectively enrolled 39 patients undergoing cardiac surgery to screen for SDB and collected right atrial appendage biopsies. Results: SDB was diagnosed in 14 patients (36%). SDB patients had significantly increased levels of oxidized and activated CaMKII (assessed by Western blotting/specific pulldown). Moreover, SDB patients showed a significant increase in Ca spark frequency (CaSpF measured by confocal microscopy) compared with control subjects. CaSpF was 3.58 ± 0.75 (SDB) vs. 2.49 ± 0.84 (no SDB) 1/100 µm−1s−1 (p &lt; 0.05). In linear multivariable regression models, SDB severity was independently associated with increased CaSpF (B [95%CI]: 0.05 [0.03; 0.07], p &lt; 0.001) after adjusting for important comorbidities. Interestingly, 30 min exposure to the CaMKII inhibitor autocamtide-2 related autoinhibitory peptide normalized the increased CaSpF and eliminated the association between SDB and CaSpF (B [95%CI]: 0.01 [−0.1; 0.03], p = 0.387). Conclusions: Patients with SDB have increased CaMKII oxidation/activation and increased CaMKII-dependent CaSpF in the atrial myocardium, independent of major clinical confounders, which may be a novel target for treatment of atrial arrhythmias in SDB.</jats:p>
  • Zugangsstatus: Freier Zugang