OBESE, DILATED CARDIOMYOPATHY, SYMPTOMATIC AORTIC STENOSIS
The expression of total HSPB5 and HSPB1 was similar in the hearts of lean, vehicle‐treated, and GGA‐treated obese ZSF1 rats. However, GGA treatment increased HSPB5 and HSPB1 in the myofilament fraction of cardiomyocytes. The increase in myofilament‐bound HSPs induced by GGA was particularly evident for HSPB1, which showed a 2.5‐fold increase in the GGA‐treated obese ZSF1 rats. The primarily myofilament localization of both small HSPs was confirmed by immunofluorescence staining. This redistribution is functionally important, as the effect of GGA on cardiomyocyte FIn a previous study, we observed a similar association of HSPB5 with the myofilaments in LV cardiomyocytes of end‐stage dilated cardiomyopathy and symptomatic aortic stenosis patients, although their association in the present study was more pronounced (Franssen et al., Titin is a large protein found in sarcomeres that responds rapidly to physiological and pathological load by altering its compliance (Sequeira et al., 