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The dose-dependent activation of the FAK-paxillin pathway has been documented in multiple studies
doi: 10.1007/s007260050001
Precursors of GSH or GPX biosynthesis, various small molecule activators related to the GSH system and some novel therapeutic approaches, such as exosomes and gene therapy, can boost the activity of the GSH system and reduce cardiac damage and ferroptosis
[1] [6] The effectiveness of this mechanism depends entirely on the active ingredient maintaining its chemical stability and potency
