3D bioprinting is a rapidly evolving industry that has been utilized for a variety of biomedical applications. It differs from traditional 3D printing in that it utilizes bioinks comprised of cells and other biomaterials to allow for the generation of complex functional tissues. Bioprinting involves computational modeling, bioink preparation, bioink deposition, and subsequent maturation of printed products; it is an intricate process where bioink composition, bioprinting approach, and bioprinter type must be considered during construct development. This technology has already found success in human studies, where a variety of functional tissues have been generated for both in vitro and in vivo applications. Although the main driving force behind innovation in 3D bioprinting has been utility in human medicine, recent efforts investigating its veterinary application have begun to emerge. To date, 3D bioprinting has been utilized to create bone, cardiovascular, cartilage, corneal and neural constructs in animal species. Furthermore, the use of animal-derived cells and various animal models in human research have provided additional information regarding its capacity for veterinary translation. While these studies have produced some promising results, technological limitations as well as ethical and regulatory challenges have impeded clinical acceptance. This article reviews the current understanding of 3D bioprinting technology and its recent advancements with a focus on recent successes and future translation in veterinary medicine.

The hypoxia‐inducible factors (HIF)‐1α and HIF‐2α are central regulators of transcriptional programmes in settings such as development and tumour expansion. HIF‐2α moonlights as a cap‐dependent translation factor. We provide new insights into how the interferon‐stimulated gene 15 (ISG15), a ubiquitin‐like modifier, and the HIFs regulate one another in hypoxia and interferon‐induced cells. We show that upon ISGylation induction and HIF‐α stabilization, both HIFs promote protein ISGylates through transcriptional and/or post‐transcriptional pathways. We show the first evidence of HIF‐2α modification by ISG15. ISGylation induces system‐level alterations to the HIF transcriptional programme and increases the cytoplasmic/nuclear fraction and translation activity of HIF‐2α. This work identifies ISG15 as a regulator of hypoxic mRNA translation, which has implications for immune processes and disease progression.