About 850 million people worldwide suffer from kidney disease, but women seem to be more likely to resist kidney disease than men, although the reasons for this are not yet clear.
A recent study published in Cell Reports suggests that there are molecular mechanisms in women that protect damaged kidney cells from cell death, which could be a new therapeutic target.
Using mouse experiments, researchers found that divalent iron ions and oxides put damaged kidney cells under stress and cause “iron death,” a key cause of kidney disease.
Using genetic and single-cell RNA transcriptome analysis in mice, the researchers found that women have a highly active nuclear factor carotenoid 2-related factor 2 (NRF2), which regulates the expression of antioxidant proteins.
It regulates the expression of antioxidant proteins and blocks the iron death pathway in kidney cells.
However, in men, testosterone reduced NRF2 activity and thus failed to block iron death.
Further experiments showed that activation of NRF2 reversed iron death in male kidney cells.
This also suggests that NRF2 may be a potential therapeutic target for the prevention of renal failure.
