TGF-β1-triggered maladaptive bone marrow endothelium impedes hematopoietic recovery.

ABSTRACT: Endothelial cells (ECs) form a critical bone marrow (BM) niche for hematopoietic stem cell regulation in homeostasis and stress states. However, BM ECs are frequently disrupted in hematologic diseases and their clinical interventions. Although transient EC injury is repairable, chronic activation of stress signals often induces maladaptive EC repair, which is a state of fibrotic reprogramming characterized by the loss of BM EC-specific functions and impaired hematopoietic-supporting ability. Although TGF-β1 (a pleiotropic cytokine) is implicated in angiogenesis and tissue repair, its role in driving BM EC maladaptation remains undefined. Here, in vitro experiments combined with a mouse model with adeno-associated virus-mediated BM EC-specific overexpression of constitutively active TGF-βRI

SUBMITTER: Lyu ZS 

PROVIDER: S-EPMC12500950 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature