UNASSIGNED: @entity296 ( @entity296 ) is a frequent underlying cause for @entity943 and @entity1164 especially during intense exercise. The mechanisms involved remain largely unknown. The purpose of this study was to investigate how chronic endurance exercise contributes to @entity69681 (DSP) mutation-induced @entity296 pathogenesis. @entity19 with overexpression of @entity69681 , wild-type (Tg-DSP( @entity7097 )), or the @entity69682 mutant (Tg-DSP( @entity69682 )) along with control nontransgenic (NTg) littermates were kept sedentary or exposed to a daily running regimen for 12 wk. Cardiac function and morphology were analyzed using echocardiography, electrocardiography, histology, immunohistochemistry, RNA, and protein analysis. At baseline, 4-wk-old @entity19 from all groups displayed normal cardiac function. When subjected to exercise, all @entity19 retained normal cardiac function and left ventricular morphology; however, Tg-DSP( @entity69682 ) mutants displayed right ventricular (RV) dilation and wall thinning, unlike NTg and Tg-DSP( @entity7097 ). The Tg-DSP( @entity69682 ) hearts demonstrated focal fat infiltrations in RV and cytoplasmic aggregations consisting of @entity69681 , plakoglobin, and @entity16899 . These aggregates coincided with disruption of the intercalated disks, intermediate filaments, and microtubules. Although Tg-DSP( @entity69682 ) @entity19 already displayed high levels of p- @entity6913 (Ser9) and p- @entity1994 (Ser473) under sedentary conditions, decrease of nuclear @entity6913 and @entity1994 levels with reduced p- @entity6913 (Ser9), p- @entity1994 (Ser473), and p- @entity1994 (Ser308) and loss of nuclear junctional plakoglobin was apparent after exercise. In contrast, Tg-DSP( @entity7097 ) showed upregulation of p- @entity1994 (Ser473), p- @entity1994 (Ser308), and p- @entity6913 (Ser9) in response to exercise. Our data suggest that endurance exercise accelerates @entity296 pathogenesis in Tg-DSP( @entity69682 ) @entity19 and this event is associated with perturbed @entity1994 and @entity6913 signaling. Our study suggests a potential mechanism-based approach to exercise management in @entity1 with @entity296 .

Accelerated cardiac remodeling in XXXX @entity19 in response to endurance exercise is associated with perturbed Wnt/b-catenin signaling.

@entity1164 :: ('MESH:D016757', 'Disease') :: ['sudden cardiac death'] @entity16899 :: ('14609(Tax:10090)', 'Gene') :: ['connexin 43'] @entity1 :: ('9606', 'Species') :: ['patients'] @entity296 :: ('MESH:D009202', 'Disease') :: ['AVC', 'Arrhythmogenic ventricular cardiomyopathy'] @entity6913 :: ('56637(Tax:10090)', 'Gene') :: ['GSK3-b'] @entity19 :: ('10090', 'Species') :: ['mice', 'Transgenic mice'] @entity7097 :: ('MESH:C536751', 'Disease') :: ['WT'] @entity69682 :: ('p|SUB|R|2834|H', 'ProteinMutation') :: ['R2834H'] @entity1994 :: ('11651(Tax:10090)', 'Gene') :: ['AKT1'] @entity69681 :: ('109620(Tax:10090)', 'Gene') :: ['desmoplakin'] @entity943 :: ('MESH:D001145', 'Disease') :: ['arrhythmias']
@entity69681 :: (109620(Tax:10090),Gene) :: ['desmoplakin']
