Key result
Doxorubicin reduces CCN2 protein levels and modulates TGF-β signaling in mouse fibroblasts.
Why the study?
The specific impact of doxorubicin on cardiac fibroblasts and its modulation of the TGF-β signaling pathway remain incompletely understood.
Does doxorubicin modulate the TGF-β signaling cascade in mouse fibroblasts?
Population
Mouse embryonic fibroblasts (NIH3T3) and mouse primary cardiac fibroblasts
Comparison
DOX treatment in the presence of TGF-β1
Design
In vitro preclinical laboratory study
Authors
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Doxorubicin's fibroblast effects are hypothesis-generating; leaves open translation to human cardiotoxicity or fibrosis pathways.
Does doxorubicin modulate the TGF-β signaling cascade in mouse fibroblasts?
p-value: p=<0.05
Doxorubicin exhibits cell-specific modulation of the TGF-β signaling pathway, reducing CCN2 in both embryonic and cardiac fibroblasts but altering other fibrotic genes primarily in embryonic fibroblasts.
Patricelli et al. (2023) studied Doxorubicin-induced cardiotoxicity (in vitro model). Doxorubicin vs. Vehicle control was evaluated on CCN2 protein expression (p=<0.05). Doxorubicin induced a dose-dependent reduction in CCN2 protein levels and modulated TGF-β signaling in a cell-specific manner in mouse fibroblasts.
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