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This study found that finasteride competitively inhibits the enzyme AKR1D1 with low micromolar affinity but does not act as a mechanism-based inactivator.

This study found that manipulating AKR1D1 expression in human liver cells effectively regulates glucocorticoid clearance and receptor activation, highlighting its role in liver-specific steroid hormone regulation.

This study provided the first X-ray crystal structure of the mammalian steroid hormone reductase AKR1D1 and identified a disease-related mutant, P133R, which may impact bile acid metabolism and cause clinical symptoms.

AKR1B10 enzyme may cause keloid scars and could be a treatment target.

This study found that uric acid-linked microvascular dysfunction may play a role in alopecia areata, suggesting that targeting endothelial function and uric acid regulation could be a potential management strategy.