Bone morphogenetic protein 8b (bmp8b) in non-alcoholic steatohepatitis (nash), acute hepatic damage and liver regeneration

TGFβ/BMP family member Bone Morphogenetic Protein 8b (Bmp8b) is upregulated in NASH (Western Diet -WD- Model), acute liver damage (CCl4 model) and by Partial Hepatectomy (PH). Absence of Bmp8b reduces liver inflammation and fibrosis in the NASH model (WD). In the acute (3days) CCl4 model, absence of Bmp8b impacts acute inflammatory responses, hepatic stellate cells (HSC) activation, and compensatory hepatocyte proliferation; defective inflammatory pathways and hepatocytes proliferation is also observed in the Partial hepatectomy model. BMP8b is thus a pathophysiologically relevant target to modulate the responses to damage in acute and chronic liver disease.

转化生长因子β/骨形态发生蛋白（TGF-β/BMP）家族成员骨形态发生蛋白8b（Bone Morphogenetic Protein 8b，Bmp8b）在非酒精性脂肪性肝炎（NASH，西式饮食（WD）模型）、急性肝损伤（四氯化碳（CCl4）模型）及部分肝切除术（PH）模型中表达上调。Bmp8b缺失可减轻NASH模型（WD模型）中的肝脏炎症与纤维化。在急性（3天）CCl4模型中，Bmp8b缺失会影响急性炎症应答、肝星状细胞（HSC）活化与肝细胞代偿性增殖；在部分肝切除术模型中，同样可观测到炎症通路缺陷与肝细胞增殖异常。综上，BMP8b是调控急慢性肝脏疾病中损伤应答的病理生理学相关靶点。