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Volume 25 Issue 5, May 2023

Wound repair memory

Epidermal injury elicits the priming of distant memory progenitors that have not contributed to original healing but acquire enhanced repair abilities, favouring field cancerization.

See Levra Levron et al. and News & Views by Lyko

Image: Image courtesy of Chiara Levra Levron and Giacomo Donati, University of Turin, Torino, Italy. Cover Design: Lauren Heslop.

News & Views

  • The Mediterranean diet correlates with increased human lifespan; it is rich in foods with high levels of cis-monounsaturated fatty acids (MUFAs), such as olive oil. A study now shows that MUFAs stimulate a lipid droplet–peroxisome organelle network to decrease lipid oxidation and protect cell membranes during ageing.

    • Alexander Richard Mendenhall
    News & Views


  • Coordination of protein quality control processes across organelles is poorly understood. A study now shows that the cytosolic juxtanuclear quality control (JUNQ) and intranuclear quality control (INQ) compartments face each other on opposite sides of the nuclear envelope before their vacuolar degradation, promoting proteostasis.

    • Simon Alberti
    • Serena Carra
    News & Views
  • Skin wounds induce an epigenetic memory that accelerates the healing of subsequent injuries. The underlying mechanism is now shown to involve epigenetic chromatin modifications in stem cells from a field of distal hair follicles that surround the injury. Importantly, this mechanism also results in a predisposition for skin cancer development.

    • Frank Lyko
    News & Views
  • The selenoprotein glutathione peroxidase 4 (GPX4) is the guardian of ferroptosis, a form of cell death earmarked by unrestrained lipid peroxidation. A new study shows that the metabolic enzyme creatinine kinase B (CKB) phosphorylates GPX4, which may influence the susceptibility of cancer cells to ferroptosis.

    • Eikan Mishima
    • Marcus Conrad
    News & Views
  • The cGAS–STING cytosolic double-stranded-DNA-sensing pathway provides protection against infection but also contributes to inflammatory pathology and thus must be tightly regulated. In this issue, Jie et al. find that endoplasmic-reticulum-associated degradation of the adaptor STING by SEL1L–HRD1 controls steady-state STING levels to limit STING-driven inflammation.

    • Kevin MingJie Gao
    • Katherine A. Fitzgerald
    News & Views
  • Direct conversions offer an alternative approach to generate insulin-producing cells for cell therapy in diabetes. A study reports a method to convert human stomach-derived gastric stem cells into functional insulin-producing cells through a unique differentiation path.

    • Jinhyuk Choi
    • Fritz Cayabyab
    • Eiji Yoshihara
    News & Views
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Research Briefings

  • Acutely damaged lysosomes can regenerate themselves by repurposing damaged membranes. After damage, cytosolic TBC1D15 relocalizes to impaired lysosomes and assembles the autophagic lysosomal reformation machinery to drive this regeneration. This mechanism exemplifies an immediate cellular response to mitigate the crisis of severe lysosomal damage.

    Research Briefing
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Technical Reports

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Amendments & Corrections

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