Corneal endothelial cells act as an ion pump and barrier to maintain corneal transparency and normal physiological function.Once injured, adult corneal endothelial cells are compensated by the migration and expansion of peripheral cells.Excessive injury leads to corneal endothelial decompensation, resulting in corneal edema and visual loss.At present, the common treatment is corneal endothelial transplantation.In recent years, the mechanism of endothelial cell proliferation, differentiation and adhesion has been extensively studied.Alternative therapies for corneal transplantation have also been proposed, including endothelial cell regeneration, induced pluripotent stem cell differentiation, cell transplantation, tissue engineering, and artificial endothelial layer.Cell transplantation and artificial endothelial layer have been approved for clinical trials, while others are still in the basic research stage and their clinical effects are still uncovered.This article reviews the research progress on corneal endothelial cell decompensation in order to find a solution to the shortage of corneal donors and to achieve clinical transformation of scientific research results as soon as possible.

Corneal endothelial cells act as an ion pump and barrier to maintain corneal transparency and normal physiological function.Once injured, adult corneal endothelial cells are compensated by the migration and expansion of peripheral cells.Excessive injury leads to corneal endothelial decompensation, resulting in corneal edema and visual loss.At present, the common treatment is corneal endothelial transplantation.In recent years, the mechanism of endothelial cell proliferation, differentiation and adhesion has been extensively studied.Alternative therapies for corneal transplantation have also been proposed, including endothelial cell regeneration, induced pluripotent stem cell differentiation, cell transplantation, tissue engineering, and artificial endothelial layer.Cell transplantation and artificial endothelial layer have been approved for clinical trials, while others are still in the basic research stage and their clinical effects are still uncovered.This article reviews the research progress on corneal endothelial cell decompensation in order to find a solution to the shortage of corneal donors and to achieve clinical transformation of scientific research results as soon as possible.

Objective : To investigate the expression levels and potential clinical significance of pre-B-cell leukemia homologous box 3 (PBX3) in bone marrow samples from acute myeloid leukemia (AML) . Methods : The mRNA expression levels of PBX3 were determined by bioinformatics which analyzed the RNAseq data of 33 malignancies from the cancer genome atlasdatabase． (TCGA) The correlations among the expression levels of PBX3，the clinical parameters and prognosis of AML patients were further analyzed．The differentially expressed genes in the whole transcriptome were analyzed to identify the molecular network in AML caused by PBX3 expression abnormalities. Results : The mRNA expression levels of PBX3 were up-regulated in 12 malignancies，and the altitudes increased most significantly in AML than any other cancer types．Patients with high PBX3 expression showed shorter overall survival and disease-free survival than patients with low PBX3 expression．High PBX3 expression was significantly associated with FLT3，NPM1，and DNMT3A mutation．PBX3 expression was positively correlated with multiple ho- meobox genes (including most HOXA and HOXB genes ，MEIS1 ) ，and the expression levels of these homeobox genes were all negatively correlated with AML patients overall survival． Conclusion PBX3 high expression in the bone marrow of AML patients is a potential biomarker for poor prognosis ，and it may have extensive interactions with other homeobox genes.