Complement C3-driven stromal reprogramming in MPN

Current understanding

To be populated as evidence accumulates.

2026-07-09 — Glutamate accumulation in myelofibrosis microenvironment rewires mesenchymal stromal cells metabolic and epigenetic profiles.: cross-connection with glutamate-mglur5-fumarate-msc-rewiring: Both describe non-cytokine microenvironmental cues (complement C3 vs glutamate/mGluR5) that reprogram MPN stromal cells toward a fibrogenic phenotype, suggesting convergent stromal-reprogramming mechanisms with distinct upstream ligands. (novelty: 5)
2026-08-03 — Spatially resolved transcriptomic profiling of myelofibrosis spleen reveals compartment specific niche programs.: cross-connection with mf-spleen-spatial-niche-compartments: Both spatial studies of MF spleen converge on compartment-organized immune-stromal niches; the C3 stromal reprogramming axis likely operates within the perivascular fibro-remodeling compartment identified here. (novelty: 4)
2026-08-25 — Spatial profiling of the spleen in mouse and human myelofibrosis reveals complement-driven immune-stromal interactions as a therapeutic target.: Spatial transcriptomic profiling of mouse and human myelofibrotic spleens identifies C3-dependent reprogramming of splenic reticular cells into inflammatory pro-fibrotic states as a driver of extramedullary niches, with genetic or pharmacologic C3 blockade reducing splenomegaly and marrow fibrosis (preclinical). (novelty: 5)