Key result
Angptl3 deficiency in mice led to decreased hematopoietic stem cell number, quiescence, and repopulation activity, indicating Angptl3 supports HSC stemness in the bone marrow niche.
Population
Angptl3-null mice and their hematopoietic stem cells (HSCs)
Design
Preclinical
Authors
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Angptl3 inhibition may impair HSC function in mice; leaves open its role in human hematopoiesis and requires clinical validation.
Angptl3 acts as an extrinsic factor in the bone marrow niche to support the stemness and repopulation activity of hematopoietic stem cells by repressing Ikaros expression.
Zheng et al. (2010) studied Hematopoietic stem cell function. Angptl3 deficiency vs. Wild-type (implied) was evaluated on Hematopoietic stem cell number, quiescence, and repopulation activity. Angptl3 deficiency in mice led to decreased hematopoietic stem cell number, quiescence, and repopulation activity, indicating Angptl3 supports HSC stemness in the bone marrow niche.
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