Table 2.

Transgenic mouse models showing the role of FoxM1 in organ injury

Mouse model	Affected cells	Injury/organ	Phenotype
Albumin-Cre Foxm1fl/fl	Deletion in hepatocytes	Partial hepatectomy/Livers	Mice showed diminished proliferation of hepatocytes after partial hepatectomy53
Tie2-Cre Foxm1fl/fl	Deletion in endothelial cells	LPS treatment/Lungs	Reduced vascular repair, decreased proliferation of endothelial cells and impaired reannealing of endothelial adherens junctions were found.45,78
Pdx1-Cre Foxm1fl/fl	Deletion in pancreatic epithelial cells	Partial pancreatectomy/Pancreas	Mice showed decreased proliferation of alpha- and beta-cells following partial pancreatectomy. No differences in proliferation of acinal or ductal cells were found.47
		Pregnancy/Pancreas	Gestational diabetes was observed in female mice during pregnancy57
mLyz-Cre Foxm1fl/fl	Deletion in macrophages and granulocytes	Carbon tetrachloride/Liver	No defects were found in macrophages and granulocytes of bone marrow and peripheral blood. Following acute liver injury by carbon tetrachloride, a delay in liver repair was found. Mice showed decreased recruitment of monocytes into the injured liver, as well as impaired differentiation of monocytes toward mature macrophage lineage.43
Rosa26-FoxM1b	Overexpression in all cell types	BHT treatment/Lungs	Increased proliferation of respiratory epithelial, endothelial and smooth muscle cells was found after BHT-mediated lung injury.44
TTR-FoxM1b	Overexpression in hepatocytes	Partial hepatectomy or carbon tetrachloride/Liver	Increased proliferation of hepatocytes was found after partial hepatectomy46 or carbon tetrachloride-mediated liver injury.48
		Partial hepatectomy and aging/Liver	Expression of FoxM1b resulted in protection of old mice against age-associated decline in liver regeneration.62