Publications by authors named "Yejun Dong"
Article Synopsis
- Endothelial dysfunction is a problem in diabetes that can lead to heart and brain diseases, and it’s influenced by changes in the way genes are controlled.
- In a study, researchers found that a protein called ASH2L increases when there is high sugar, causing damage to blood vessels in diabetic mice and cells.
- They discovered that reducing ASH2L levels could help protect blood vessels from this damage, suggesting that blocking ASH2L might be a way to treat blood vessel problems in diabetes.
Ischemic stroke is known to cause the accumulation of misfolded proteins and loss of calcium homeostasis, leading to impairment of endoplasmic reticulum (ER) function and activating the unfolded protein response (UPR). PARP16 is an active (ADP-ribosyl)transferase known tail-anchored ER transmembrane protein with a cytosolic catalytic domain. Here, we find PARP16 is highly expressed in ischemic cerebral hemisphere and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated immortalized hippocampal neuronal cell HT22.
View Article and Find Full Text PDFDiabetic nephropathy (DN) is a leading cause of end-stage renal disease and continues to be a threat to patients with diabetes. Dysfunction of glomerular mesangial cells (GMCs) is the main contributing factor to glomerulosclerosis, which is a pathological feature of DN. The epigenetic factor ASH2L has long been thought to be a transcriptional activator, but its function and involvement in diabetic nephropathy is still unclear.
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