Fig. 2.

Ibrutinib promotes electrical remodeling associated with atrial fibrillation (AF) development. (A–B) Representative recordings of transient Ca²⁺ changes (n = 10 cells per group, Student's t-test) and the sarcoplasmic reticulum (SR) Ca²⁺ content (n = 5 cells per group, Student's t-test). (C–G) Quantification of the amplitude, decay time, time to peak of calcium release, and the amplitude of caffeine-induced Ca²⁺ release between the control and ibrutinib-treated groups (n = 10 cells per group; Student's t-test). (H–K) Representative line-scan confocal images and the quantification of Ca²⁺ sparks (CaSF) in control group mice and ibrutinib group mice (n = 10 cells per group; Student's t-test). FDHM, spark duration; FWHD, spark width. (L) Representative images showing the MitoSOX fluorescence intensity in a single atrial myocyte at different times (n = 5 cells per group). Scale bar: 50 μm. (M) Quantification of mitochondrial reactive oxygen species (ROS) production in the control group, ibrutinib group, and DL-Dithiothreitol (DTT) group (n = 5 cells per group; one way ANOVA). Values are presented as mean ± SD. *P < 0.05, **P < 0.01 vs Control group.