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This finding reveals a complex interactive network between copper dyshomeostasis, oxidative stress, and distinct programmed cell death pathways involved in cardiac pathology

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The homocysteine-inducible, endoplasmic reticulum (ER) stress-inducible, ubiquitin-like domain member 2 (HERPUD1) in cultured HELA cells facilitate cytoprotective effects against oxidative stress by suppressing the inositol 1,4,5-triphosphate receptor and reducing the transfer of calcium ions from the endoplasmic reticulum to mitochondria [41]

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