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The actin cytoskeleton lies at the heart of many essential cellular processes. There are hundreds of proteins that cells use to control the size and shape of actin cytoskeletal networks. As such, various pathogens utilize different strategies to hijack the infected eukaryotic host actin dynamics for their benefit. These include the control of upstream signaling pathways that lead to actin assembly, control of eukaryotic actin assembly factors, encoding toxins that distort regular actin dynamics, or by encoding effectors that directly interact with and assemble actin filaments. The latter class of effectors is unique in that, quite often, they assemble actin in a straightforward manner using novel sequences, folds, and molecular mechanisms. The study of these mechanisms promises to provide major insights into the fundamental determinants of actin assembly, as well as a deeper understanding of host–pathogen interactions in general, and contribute to therapeutic development efforts targeting their respective pathogens. This review discusses mechanisms and highlights shared and unique features of actin assembly by pathogen effectors that directly bind and assemble actin, focusing on eukaryotic actin nucleator functional mimics Rickettsia Sca2 (formin mimic), Burkholderia BimA (Ena/VASP mimic), and Vibrio VopL (tandem WH2-motif mimic). [ABSTRACT FROM AUTHOR]

Among advanced therapy medicinal products, tissue-engineered products have the potential to address the current critical shortage of donor organs and provide future alternative options in organ replacement therapy. The clinically available tissue-engineered products comprise bradytrophic tissue such as skin, cornea, and cartilage. A sufficient macro- and microvascular network to support the viability and function of effector cells has been identified as one of the main challenges in developing bioartificial parenchymal tissue. Three-dimensional bioprinting is an emerging technology that might overcome this challenge by precise spatial bioink deposition for the generation of a predefined architecture. Bioinks are printing substrates that may contain cells, matrix compounds, and signaling molecules within support materials such as hydrogels. Bioinks can provide cues to promote vascularization, including proangiogenic signaling molecules and cocultured cells. Both of these strategies are reported to enhance vascularization. We review pre-, intra-, and postprinting strategies such as bioink composition, bioprinting platforms, and material deposition strategies for building vascularized tissue. In addition, bioconvergence approaches such as computer simulation and artificial intelligence can support current experimental designs. Imaging-derived vascular trees can serve as blueprints. While acknowledging that a lack of structured evidence inhibits further meta-analysis, this review discusses an end-to-end process for the fabrication of vascularized, parenchymal tissue. [ABSTRACT FROM AUTHOR]