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Iron overload following ischemia may be mediated through two primary pathways: IL-6JAK/STAT3hepcidin axis: Ischemia-induced IL-6 activates the JAK/STAT3 signaling pathway, which enhances hepcidin expression

Porbski et al

This article provides an excellent overview of clinical DDIs in the kidney

Once in the tissues, ALA can be found inside and outside the cells including inside the mitochondria where it functions naturally as a coenzyme for the oxidation of pyruvate, alpha ketoglutarate, and branched-chain amino acids.*

Both peptides have strong individual safety profiles, their mechanisms don't conflict, and clinical experience with the combination hasn't revealed unexpected adverse effects