Figure 1.
Pathways of megakaryopoiesis, highlighting key mechanisms of communication within the BM niche. (A) Canonical megakaryopoiesis involves differentiation through LT-HSCs, ST-HSCs, and MPPs (MPP2, MPP3, MPP4, and MPP5). In the first bifurcation, MPPs differentiate into CMPs or common lymphoid progenitors (CLP). Continuing down the myeloid lineage, CMPs can then differentiate into granulocyte-macrophage progenitors (GMP) as well as MEPs. MEPs can then differentiate to MkPs that terminally differentiate into MKs. The MK-biased pathway and stem-like MK-committed progenitors (SL-MkP), are highlighted here using an arrow. (B) MKs interact with their surrounding cells, such as adipocytes. MKs uptake fatty acids (FA) released by adipocytes via a CD36-dependent mechanism to facilitate their maturation. (C) Secreted molecules, such as growth factors, cytokines, and lipids, help to orchestrate and maintain the hematopoietic response. (D) PEVs can leave the circulation and infiltrate the BM, where they bind to resident BM cells, including HSCs and MKs, and affect their development.

Pathways of megakaryopoiesis, highlighting key mechanisms of communication within the BM niche. (A) Canonical megakaryopoiesis involves differentiation through LT-HSCs, ST-HSCs, and MPPs (MPP2, MPP3, MPP4, and MPP5). In the first bifurcation, MPPs differentiate into CMPs or common lymphoid progenitors (CLP). Continuing down the myeloid lineage, CMPs can then differentiate into granulocyte-macrophage progenitors (GMP) as well as MEPs. MEPs can then differentiate to MkPs that terminally differentiate into MKs. The MK-biased pathway and stem-like MK-committed progenitors (SL-MkP), are highlighted here using an arrow. (B) MKs interact with their surrounding cells, such as adipocytes. MKs uptake fatty acids (FA) released by adipocytes via a CD36-dependent mechanism to facilitate their maturation. (C) Secreted molecules, such as growth factors, cytokines, and lipids, help to orchestrate and maintain the hematopoietic response. (D) PEVs can leave the circulation and infiltrate the BM, where they bind to resident BM cells, including HSCs and MKs, and affect their development.

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