Autophagy is a universal cellular homeostatic process, required for the clearance of dysfunctional macromolecules or organelles. This self-digestion mechanism modulates cell survival, either directly by targeting cell death players, or indirectly by maintaining cellular balance and bioenergetics. Nevertheless, under acute or accumulated stress, autophagy can also contribute to promote different modes of cell death, either through highly regulated signalling events, or in a more uncontrolled inflammatory manner. Conversely, apoptotic or necroptotic factors have also been implicated in the regulation of autophagy, while specific factors regulate both processes. Here, we survey both earlier and recent findings, highlighting the intricate interaction of autophagic and cell death pathways. We, Furthermore, discuss paradigms, where this cross-talk is disrupted, in the context of disease.
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Cover Image
Cover Image
In this issue Oldham and colleagues (pp. 57–74) have performed extensive structural and kinetic characterization of the SAT enzyme from the antibiotic-resistant pathogen Neisseria gonorrhoeae. Using X-ray crystallography, we have solved the structures of NgSAT with the non-natural ligand, l-malate. They present data which could be explored to combat the rise of antimicrobial resistant N. gonorrhoeae. The cover image shows a ribbon diagram of the NgSAT trimer illustrating the position and formation of the active site between two adjacent monomers. The image is courtesy of Joanna Hicks.
The complex interplay between autophagy and cell death pathways
Christina Ploumi, Margarita-Elena Papandreou, Nektarios Tavernarakis; The complex interplay between autophagy and cell death pathways. Biochem J 14 January 2022; 479 (1): 75–90. doi: https://doi.org/10.1042/BCJ20210450
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