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The United Nations (UN) 2030 Sustainable Development Agenda, signed in 2015 and backed-up with its seventeen Sustainable Development Goals (SDGs), mentions cities as key players for evolving actively towards more sustainability. This underpins that living in the cities of the urban age is increasingly becoming the focus of sustainability discussions, which is particularly reflected in SDG 11 “Making cities and human settlements inclusive, safe, resilient and sustainable„. As urban sustainability strategies are playing a key role for the development of cities, this article sheds light on four cities’ sustainability strategies. The case studies highlight shortcomings, in terms of integrated visions, clear targets, and indicators in existing urban (sustainability) strategies. The article discusses these issues in light of an analytical framework, and stresses challenges and opportunities that SDG implementation involves.

The cytokines secreted by immune cells have a large impact on the tissue, surrounding a fracture, e.g., by attraction of osteoprogenitor cells. However, the underlying mechanisms are not yet fully understood. Thus, this study aims at investigating molecular mechanisms of the immune cell-mediated migration of immature primary human osteoblasts (phOBs), with transforming growth factor beta (TGF-&beta, ), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) and focal adhesion kinase (FAK) as possible regulators. Monocyte- and macrophage (THP-1 cells &plusmn, phorbol 12-myristate 13-acetate (PMA) treatment)-conditioned media, other than the granulocyte-conditioned medium (HL-60 cells + dimethyl sulfoxide (DMSO) treatment), induce migration of phOBs. Monocyte- and macrophage (THP-1 cells)-conditioned media activate Smad3-dependent TGF-&beta, signaling in the phOBs. Stimulation with TGF-&beta, promotes migration of phOBs. Furthermore, TGF-&beta, treatment strongly induces NOX4 expression on both mRNA and protein levels. The associated reactive oxygen species (ROS) accumulation results in phosphorylation (Y397) of FAK. Blocking TGF-&beta, signaling, NOX4 activity and FAK signaling effectively inhibits the migration of phOBs towards TGF-&beta, In summary, our data suggest that monocytic- and macrophage-like cells induce migration of phOBs in a TGF-&beta, dependent manner, with TGF-&beta, dependent induction of NOX4, associated production of ROS and resulting activation of FAK as key mediators.