Key result
DDR2-mediated ERK1/2 MAPK activation facilitates coordinated regulation of cell survival and cell cycle progression in cardiac fibroblasts via SRF.
Why the study?
Cardiac fibroblast-specific factors and mechanisms underlying apoptosis resistance, proliferation, and scar formation during wound healing and tissue remodeling after myocardial injury remain to be identified.
Population
Cardiac fibroblasts, including from Spontaneously Hypertensive Rats
Comparison
Gene knockdown and over-expression approaches, and DDR2 inhibition with WRG-28
Design
In vitro experimental study
Authors
Loading...
May identify fibroblast targets for post-MI repair; leaves open clinical translation pending validation.
DDR2 plays a crucial role in cardiac fibroblast survival and proliferation following injury by coordinating apoptosis resistance and cell cycle progression via the ERK1/2 MAPK and SRF pathways.
Titus et al. (2019) studied Myocardial injury. DDR2 gene knockdown, over-expression, and WRG-28 inhibition was evaluated on Regulation of cell survival and cell cycle pathways (expression of cIAP2, Skp2, p27, PCNA). DDR2-mediated ERK1/2 MAPK activation facilitates coordinated regulation of cell survival and cell cycle progression in cardiac fibroblasts via SRF.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: