Key result
STAT1 and STAT3 mediate high glucose-induced proliferation and collagen synthesis in cardiac fibroblasts, and both have synergetic effects with ERK1/2 on regulating these processes.
Population
Rat cardiac fibroblasts (CFs) cultured in vitro
Comparison
High glucose with or without STAT1 inhibitor… vs Normal glucose or high glucose without inhibitors
Design
Preclinical
Authors
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May nominate STAT1/STAT3-ERK1/2 as antifibrotic targets in hyperglycemia; leaves open in vivo and clinical translation.
STAT1 and STAT3 synergistically regulate high glucose-induced cardiac fibroblast proliferation and collagen synthesis with ERK1/2 in vitro.
Dai et al. (2013) studied High glucose-induced cardiac fibrosis. STAT1 inhibitor Fludarabine, STAT3 inhibitor S31-201, and ERK1/2 inhibitor PD98059 vs. High glucose without inhibitors was evaluated on Proliferation of cardiac fibroblasts and collagen types I and III synthesis. STAT1 and STAT3 mediate high glucose-induced proliferation and collagen synthesis in cardiac fibroblasts, and both have synergetic effects with ERK1/2 on regulating these processes.
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