Key result
SMC-specific ablation of GC-B in mice did not alter total atherosclerotic lesion area but promoted a more fibrotic and osteochondrogenic plaque phenotype with increased chondrocyte-like cells.
Why the study?
Balanced cGMP signaling maintains cardiovascular homeostasis, but the role of natriuretic peptide signaling pathways in VSMCs during atherogenesis required investigation.
Does silencing the CNP/GC-B axis in murine VSMCs increase their transition to chondrocyte-like plaque cells?
Population
Murine VSMCs and atherosclerotic lesions
Comparison
Silencing of the CNP/GC-B axis in VSMCs vs control
Design
Preclinical single-cell profiling and silencing study
Authors
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Animal data suggest GC-B protects against osteochondrogenic plaque shift; leaves open clinical relevance in human atherosclerosis.
Does silencing the CNP/GC-B axis in murine VSMCs increase their transition to chondrocyte-like plaque cells?
The CNP/GC-B/cGMP pathway acts as an atheroprotective regulator in VSMCs, limiting their transition to chondrocyte-like cells during atherosclerosis.
Lehners et al. (2025) studied Atherosclerosis. SMC-specific GC-B ablation vs. Control mice was evaluated on Atherosclerotic lesion area and plaque composition. SMC-specific ablation of GC-B in mice did not alter total atherosclerotic lesion area but promoted a more fibrotic and osteochondrogenic plaque phenotype with increased chondrocyte-like cells.
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