IL1 and megakaryotyces in obesity

Schematic of the effects of interleukin (IL)1-beta/IL1R1 on megakaryocyte and platelet function. A high fat diet will cause megakaryocytes to produce platelets with an increase in both inflammatory and thrombotic genes. IL1-beta in circulation as a result of increased body weight will bind IL1R1 on megakaryocytes. This interaction leads to the activation of the nuclear factor (NF)kB, PI3K/Akt, and mitogen activated protein kinase (MAPK) (ERK and p38) pathways. As a result, there is an increase in megakarycoyte maturation, including increased adhesion, increases in ploidy, and increases in mRNA production of inflammatory and thrombotic genes. IL1-beta can also bind IL1R1 on platelets and either enhance aggregation induced by agonists or promote adhesion and heterotypic aggregate formation. Some of the data used to create the pathway was generated in mouse (noted in pathway), however the pathway represents human homologs of those genes.

该图解展示了白介素（IL）1-β/IL1R1对巨核细胞和血小板功能的影响机制。高脂肪饮食会导致巨核细胞产生血小板，并使炎症和血栓形成相关基因的表达增加。由于体重增加而循环中的IL1-β将结合巨核细胞上的IL1R1。这种相互作用导致核因子（NF）kB、PI3K/Akt和丝裂原活化蛋白激酶（MAPK）（ERK和p38）途径的激活。因此，巨核细胞的成熟度增加，包括粘附性增强、倍性增加以及炎症和血栓形成相关基因mRNA生产的增加。IL1-β还可以结合血小板上的IL1R1，从而增强由激动剂诱导的聚集，或促进粘附和异型聚集的形成。用于创建该途径的部分数据是在小鼠中生成的（在途径中注明），然而，该途径代表了人类同源基因。