Why the study?
Does heterozygosity for A-band titin truncation cause dilated cardiomyopathy and hemodynamic stress intolerance in adult zebrafish?
Does heterozygosity for A-band titin truncation cause dilated cardiomyopathy and hemodynamic stress intolerance in adult zebrafish?
Heterozygosity for A-band titin truncation is sufficient to cause dilated cardiomyopathy in adult zebrafish, suggesting that hemodynamic stress may be an important modifiable risk factor in human TTNtv-related DCM.
Titin truncation impairs diastolic function in zebrafish; leaves open hemodynamic stress as modifiable factor in human TTNtv DCM.
fish with prolonged isovolumic relaxation and increased diastolic passive stiffness in the absence of myocardial fibrosis. These defects reduced diastolic reserve under stress conditions and resulted in disproportionately greater atrial dilation than observed in wild-type fish. Conclusions Heterozygosity for A-band titin truncation is sufficient to cause DCM in adult zebrafish. Abnormalities of systolic and diastolic reserve in titin-truncated fish reduce stress tolerance and may contribute to a substrate for atrial arrhythmogenesis. These data suggest that hemodynamic stress may be an important modifiable risk factor in human TTNtv-related DCM.
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Huttner et al. (2018) studied this question.
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