Cardiomyocyte‐specific MyD88 knockout prevents STZ‐induced cardiac inflammation and injury. Male MyD88f/f and MyD88f/fMyh6Cre mice were injected with STZ to induce T1DM. A) Fasting blood glucose and B) body weight were recorded weekly for 16 weeks. Heart tissue and blood samples were collected at termination for the determination of C) heart weight/tibia length (HW/TL) ratios, D) serum LDH, and E) serum CK‐MB activity. Representative images (400X magnification) of F) H&E staining (longitudinal and transverse), G) Sirius red and Masson's trichrome staining of the heart tissues were shown (scale bar = 50 µm). Representative H) western blot and I) qPCR analysis of MyHc, Col‐1, and TGF‐β in the heart tissue were shown. J) Levels of p‐ERK/ERK, p‐JNK/JNK, and IκB‐α were determined by western blot. GAPDH was loading control. K) qPCR analyses of Tnf, Il6, and Il1b in the heart tissues were shown. All data are shown as mean ± SEM (n = 6 per group; *p < 0.05, **p < 0.01, ***p < 0.001 compared to MyD88f/f; ns = not significant, #p < 0.05, ##p < 0.01, ###p < 0.001 compared to MyD88f/f+T1DM by one‐way ANOVA followed by Bonferroni's multiple comparisons test).