Key result
Interleukin-10 inhibits bone marrow fibroblast progenitor cell homing and transdifferentiation to myofibroblasts in pressure-overloaded myocardium by suppressing Smad-miRNA-21-mediated activation.
IL10 protects against pressure overload-induced cardiac fibrosis by inhibiting the mobilization, homing, and transdifferentiation of bone marrow fibroblast progenitor cells via suppression of the Smad-miRNA-21 pathway.
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IL-10 modulation of BM-derived fibrosis in pressure overload is hypothesis-generating; leaves open translation to human HF therapies.
Verma et al. (2017) studied Pressure overload-induced cardiac fibrosis. Interleukin-10 (IL10) vs. IL10 knockout / untreated was evaluated on Bone marrow fibroblast progenitor cell mobilization, homing, and transdifferentiation to myofibroblasts. Interleukin-10 inhibits bone marrow fibroblast progenitor cell homing and transdifferentiation to myofibroblasts in pressure-overloaded myocardium by suppressing Smad-miRNA-21-mediated activation.
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