Key result
Combined Obsc and Obsl1 loss in murine hearts triggers delayed relaxation and heart failure signs.
Why the study?
The precise molecular functions, redundancies, and involvement in cardiac diseases of obscurin protein family members remain to be fully understood.
Population
Knockout mice for Obsc, Obsl1, and Obsc/Obsl1 double knockouts
Comparison
Obsc knockout vs Obsl1 knockout vs Obsc/Obsl1 double knockout
Design
Preclinical animal knockout study
Authors
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Identifies Obsc/Obsl1 as essential for murine relaxation and mitophagy; leaves open relevance to human diastolic dysfunction.
The combined loss of Obsc and Obsl1 in murine hearts causes diastolic dysfunction, altered metabolism, and deregulated mitophagy, demonstrating their essential role in cardiac sarcoplasmic reticulum and mitochondrial function.
Fujita et al. (2025) studied this question. Combined loss of Obsc and Obsl1 in murine hearts resulted in profound delayed cardiac relaxation, perturbed calcium cycling, abnormal mitophagy, and metabolic signs of heart failure.
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