Figure 4. CM-specific FKBP5-deficiency leads to the increased activity of NCX1.

(A) Representative traces of the 1 Hz-pacing induced Ca²⁺ transients (CaTs), followed by baseline recording and the caffeine (10 mmol/L) induced CaTs in atrial CMs of Ctl and cKD mice. Red arrows pointed to the spontaneous Ca²⁺ waves (SCaWs) in the atrial CM of cKD mice. (B) Incidence and (C) frequency of SCaWs in atrial CMs of Ctl and cKD mice. (D) Quantification of relative SERCA activity. (E) Quantification of relative NCX function. (F) SR Ca²⁺ load. (G) Western blots and (H) quantification of NCX1 in cytosol- and membrane-fractions of atrial tissue of Ctl and cKD mice. GAPDH and caveolin 3 (Cav3) were used as control for the cytosol- and membrane-fractions, respectively. (I) Western blots and quantification of NCX1 in cytosol (Cyto)- and membrane (Mem)-fractions of atrial tissue of NSR and cAF patients. GAPDH and Gβ were used as control for the cytosol- and membrane-fractions, respectively. (J) Representative recording of I_ti elicited by the rapid application caffeine in atrial CMs. (K) Quantification of the current density of I_ti. p-values were determined with Fisher’s exact test in B, Mann-Whitney test in C, H, and I, and multilevel mixed model in E and K.