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It has been reported that oral administration of glutathione did not change the levels of glutathione and glutathione disulfide in the deproteinized fraction of blood [10], and it has been suggested that orally administered glutathione is degraded into constituting amino acids and does not exert specific activity beyond the amino acid source
This demonstrates that treatment with liraglutide has the potential to act as a prophylactic treatment (McClean et al., 2015)
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These insights have led to the clinical exploration of the MPO inhibitor mitiperstat (AZD4831) as a promising therapeutic agent for HFpEF, targeting oxidative stress[124]
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