Key result
Mitogen-stimulated cardiac fibroblasts utilize DDR2-dependent activation of ERK1/2 MAPK and serum response factor to coordinate apoptosis resistance and cell cycle progression.
This study identifies a novel DDR2-dependent molecular pathway that promotes survival and proliferation of cardiac fibroblasts, which may be important for scar formation after myocardial injury.
May guide antifibrotic targeting post-injury; leaves open in vivo validation and human translation.
Relative resistance to apoptosis and the ability to proliferate and produce a collagen-rich scar enable cardiac fibroblasts to play a central role in myocardial response to injury. This study reports novel findings that mitogen-stimulated cardiac fibroblasts exploit a common regulatory mechanism involving collagen receptor (DDR2)-dependent activation of ERK1/2 MAPK and serum response factor to achieve coordinated regulation of apoptosis resistance and cell cycle progression, which could facilitate their survival and function in the injured myocardium.
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Titus et al. (2020) studied Myocardial injury. DDR2-dependent activation of ERK1/2 MAPK and serum response factor was evaluated on Apoptosis resistance and cell cycle progression. Mitogen-stimulated cardiac fibroblasts utilize DDR2-dependent activation of ERK1/2 MAPK and serum response factor to coordinate apoptosis resistance and cell cycle progression.
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