Citizen science and social innovation as citizen empowerment tools to address urban health challenges: The case of the urban health citizen laboratory in Barcelona, Spain.

Urban health faces significant challenges due to the rapid growth of cities and the concentration of population in urban settings that have a strong impact on people's health. The approach to characterize and address these challenges requires increased societal involvement and interdisciplinary solutions to ensure their effectiveness and democratic nature. With this purpose, it is necessary to explore methodologies for citizen participation that foster a critical understanding of the environment and promote their active role in generating scientific knowledge and change. This article describes the creation of a collaborative space for experimentation and learning that, through the intersection of citizen science and social innovation, aims to engage citizens in the research and diagnosis of their local environment, as well as in the design and implementation of local solutions, while raising awareness about the main challenges to urban health. Through a collaborative and participatory framework, the community identified relevant challenges to urban health they wanted to investigate, co-designed and developed the methodology for data collection and analysis, and ultimately, they devised, designed, and implemented innovative solutions based on the scientific evidence obtained. The framework and results of this project hold potential interest for the scientific community, facilities, institutions, and society by offering an innovative and participatory approach to addressing the present and future urban health challenges.

Proteostasis failure and mitochondrial dysfunction leads to aneuploidy-induced senescence.

Aneuploidy, an unbalanced number of chromosomes, is highly deleterious at the cellular level and leads to senescence, a stress-induced response characterized by permanent cell-cycle arrest and a well-defined associated secretory phenotype. Here, we use a Drosophila epithelial model to delineate the pathway that leads to the induction of senescence as a consequence of the acquisition of an aneuploid karyotype. Whereas aneuploidy induces, as a result of gene dosage imbalance, proteotoxic stress and activation of the major protein quality control mechanisms, near-saturation functioning of autophagy leads to compromised mitophagy, accumulation of dysfunctional mitochondria, and the production of radical oxygen species (ROS). We uncovered a role of c-Jun N-terminal kinase (JNK) in driving senescence as a consequence of dysfunctional mitochondria and ROS. We show that activation of the major protein quality control mechanisms and mitophagy dampens the deleterious effects of aneuploidy, and we identify a role of senescence in proteostasis and compensatory proliferation for tissue repair.