Hong Chen

The paper identifies a new rostral midline progenitor population in human embryos using spatial transcriptomics and shows their role in mesoendoderm induction.

The paper identifies a GATA2-PROX1-FOXC2 regulatory axis that integrates shear stress signaling with lymphatic vascular development, showing dosage-dependent cooperation between GATA2 and FOXC2.

This study identifies PCBP1's role in regulating AARS2 alternative splicing and its impact on heart development and congenital cardiomyopathy.

This study shows that epsin deletion reduces foam cell formation and rewires vascular smooth muscle cell and endothelial functions in atherosclerosis.

MEBOCOST infers metabolite-mediated cell communications from single-cell RNA-seq data, identifying known and novel interactions in mouse brown adipose tissue.

This study shows that chronic inhaled benzene exposure worsens atherosclerosis in LDLR-KO mice by increasing T-cell proliferation and Th17 polarization, along with vascular smooth muscle cell changes.

This study shows that S1PR1 regulates lymphatic valve development and prevents tertiary lymphoid organ formation in the terminal ileum, suggesting TLOs as a sign of subclinical inflammation.

This study shows that deleting CD45 in endothelial cells reduces atherosclerosis by inhibiting EndoMT and TGFβ signaling through increased FGFR2 and KLF2 expression.

SCIG identifies cell identity genes using genetic sequence signatures and single-cell RNA-seq data without comparing to other cells, revealing master transcription factors and the role of tissue microenvironment.

This study shows that targeting liver epsins reduces atherosclerosis by preventing PCSK9-mediated LDLR degradation and improving LDL-C clearance.

This study identifies Dab2 and FoxM1 as key regulators of endothelial dysfunction in diabetes, showing that restoring Dab2 improves angiogenesis and wound healing.

This paper shows that PROX1 inhibits PDGF-B expression in heart valves to prevent myxomatous degeneration, and PDGF-B inhibition ameliorates valve defects in mice.

This study identifies the AIBP-CAV1-VEGFR3 axis as a regulator of lymphangiogenesis, showing that AIBP-mediated cholesterol efflux enhances VEGFC-driven lymphatic vessel formation.

This study identifies S1PR1 as a regulator of lymphatic vessel quiescence by inhibiting LSS-dependent VEGF-C signaling in lymphatic endothelial cells.

The paper shows that vascular injury leads to changes in vessel network topology to increase blood flow and activate Notch-ephrinb2 signaling for microcirculation restoration.

This study identifies GATA2's role in maintaining lymphatic endothelial cell junctions and valve morphogenesis through regulation of miR-126.