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ARBs increase ACE, which degrades BKN, but block AT1Rs and hypertension induced dementia (Campbell et al., 1995) 3
Moreover, GSTs can physically interact with various proteins and structurally diverse non-substrate molecules, including heme, steroids, and bilirubin, thereby impacting signaling pathways and altering their activity
However, the mechanisms by which AEC2 cell dysfunction contributes to these diseases remain a challenging question (Figure 1)
doi: 10.1038/srep14174
(Suzuki and Yamamoto 2017
