Key result
SP1 mediates SFRP5 loss during atrial fibrillation by transcriptional repression, contributing to cardiac fibrosis and myocyte apoptosis, which can be mitigated by SFRP5 restoration or SP1 knockdown.
Why the study?
SFRP5 is a cardioprotective protein with diminished expression in AF, but its function in AF-related cardiac fibrosis and cardiomyocyte apoptosis and the causes of its dysregulation remained to be investigated.
Population
C57BL/6 mice, mouse cardiac fibroblasts, HC-1 atrial myocytes, and clinical patient plasma samples
Comparison
Recombinant SFRP5 or SP1 knockdown vs controls in Ang II-induced AF models
Design
Preclinical animal and in vitro mechanistic study
Authors
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SFRP5-SP1 modulation attenuates fibrosis in rodent AF; leaves open whether this axis is druggable in patients.
SP1-mediated transcriptional repression of SFRP5 contributes to AF-related cardiac fibrosis and myocyte apoptosis, highlighting the SFRP5-SP1 axis as a potential therapeutic target.
Hu et al. (2024) studied Atrial fibrillation. SFRP5 recombinant protein and SP1 knockdown vs. Angiotensin II-induced AF models was evaluated on Cardiac fibrosis and cardiomyocyte apoptosis. SP1 mediates SFRP5 loss during atrial fibrillation by transcriptional repression, contributing to cardiac fibrosis and myocyte apoptosis, which can be mitigated by SFRP5 restoration or SP1 knockdown.
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