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Xiaomeng Ren

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  22
Citations -  1205

Xiaomeng Ren is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Lung & Inflammation. The author has an hindex of 17, co-authored 21 publications receiving 959 citations.

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Journal ArticleDOI

Foxm1 transcription factor is required for lung fibrosis and epithelial‐to‐mesenchymal transition

TL;DR: Lineage‐tracing studies demonstrated that Foxm1 increased EMT during radiation‐induced pulmonary fibrosis in vivo, and it was found that siRNA‐mediated inhibition ofFoxm1 prevented TGF‐β‐induced EMT in vitro.
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FOXF1 Transcription Factor Is Required for Formation of Embryonic Vasculature by Regulating VEGF Signaling in Endothelial Cells

TL;DR: FoxF1 is required for the formation of embryonic vasculature by regulating endothelial genes critical for vascular development and vascular endothelial growth factor signaling.
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Foxf genes integrate tbx5 and hedgehog pathways in the second heart field for cardiac septation.

TL;DR: The findings implicate Foxf genes in atrioventricular septation, describe the molecular underpinnings of the genetic interaction between Hedgehog signaling and Tbx5, and establish a molecular model for the selection of the SHF gene regulatory network for cardiac septal defects are established.
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Deletion of Forkhead Box M1 transcription factor from respiratory epithelial cells inhibits pulmonary tumorigenesis.

TL;DR: expression of Foxm1 in respiratory epithelial cells is critical for lung cancer formation and TOPO-2α expression in vivo, suggesting that Foxm 1 is a promising target for anti-tumor therapy.
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Foxm1 transcription factor is required for macrophage migration during lung inflammation and tumor formation.

TL;DR: Expression of Foxm1 in macrophages is required for pulmonary inflammation, recruitment of macrophage into tumor sites and lung tumor growth, and decreased tumorigenesis was associated with diminished proliferation of tumor cells and decreased recruitment ofmacrophages during the early stages of tumor formation.