Decreased H3K9ac level of AT2R mediates the developmental origin of glomerulosclerosis induced by prenatal dexamethasone exposure in male offspring rats
Decreased H3K9ac level of AT2R mediates the developmental origin of glomerulosclerosis induced by prenatal dexamethasone exposure in male offspring rats
Authors
Keywords
Prenatal dexamethasone exposure, Glomerulosclerosis, Kidney development, Angiotensin II receptor type 2 (AT2R), Intrauterine programming, Histone acetylation
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