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[126] demonstrated that STAT3 signaling activated the expression of IDO, a major inducer of the immunosuppressive milieu, without the need for binding of STAT3 protein to the promoter of IDO gene in human MDSCs

However, research into ferroptosis mechanisms in CHD remains in its early stages, with significant questions regarding its relationship with other cell death pathways and the clinical efficacy of ferroptosis-targeting interventions requiring further investigation

[3] [17] IPF is believed to be the result of an aberrant wound healing process including/involving abnormal and excessive deposition of collagen (fibrosis) in the pulmonary interstitium with minimal associated inflammation

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