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. 2026 Sep 22;139(10):e329035. doi: 10.1161/CIRCRESAHA.126.329035

Figure 6.

An eight-panel analysis of calpain inhibition in Casq2R33Q/R33Q mice. A, western blots show CASQ2 and TRDN in neonatal cardiomyocytes treated or untreated with calpeptin. B, calpeptin increases CASQ2 and TRDN levels in mutant cells, with significant differences across treatment groups. C, western blots show alpha-fodrin and its cleavage product after MDL28170 treatment. D, MDL28170 reduces the alpha-fodrin cleavage ratio (p=0.0019). E, western blots show CASQ2, TRDN, and JCTN after MDL28170 treatment. F, MDL28170 increases CASQ2 and TRDN levels and shows a nonsignificant increase in JCTN. G, western blots show reduced GRP78 and GRP94 after MDL28170. H, quantification confirms significant reductions in both proteins (p=0.001 and p=0.001).

Calpain activity is increased in Casq2R33Q/R33Q mice. A and B, Expression of CAPN1 (calpain 1) and CAST proteins in myocardial samples from Casq2R33Q/R33Q and Casq2WT/WT mice was analyzed by Western blot (A), and the band intensity was quantified (B). Vinculin was used as a loading control. C, The degree of calpain activation was determined by analyzing cleavage of the calpain target α-fodrin (alpha-fodrin) by Western blot in myocardial samples from Casq2R33Q/R33Q and Casq2WT/WT mice. D, The intensity of Western blot bands was quantified and expressed as the α-fodrin 150/240 kDa ratio. Data are represented as fold induction±SEM over the values of Casq2WT/WT mice. B and D, Data are expressed as fold induction±SEM over the values of Casq2WT/WT mice; 2-way ANOVA with Šídák’s multiple comparisons test (B) and Mann-Whitney U test (D) were used. n=13 (B) and n=8 to 10 (D). C/α-fodrin indicates processed α-fodrin; CAPN1, calpain 1; CASQ2, calsequestrin 2; CAST, calpastatin; JCTN, junctin; and TRDN, triadin.