Mechanisms of disease articles from across Nature Portfolio

Age is a leading risk factor for osteoarthritis, a degenerative joint disease; however, the mechanisms by which degeneration occurs are not well defined. In this issue of Nature Aging, Wang, He, Gong and colleagues report that a specific palmitoyl acyl transferase, ZDHHC11, prevents cartilage degradation by modifying cellular senescence, which highlights its therapeutic potential.

Using multiplexed spatially resolved transcriptomic approaches, the authors generate a topographic atlas of the healthy adult lung with location-related gene expression variability or neighbourhood changes as exemplified by COPD patient sample analysis.

Results of an early-phase breast cancer prevention trial demonstrate the potential for breast cancer prevention in premenopausal women with anti-progestin therapy by inducing epithelial–stromal remodelling and suppression of luminal progenitors.

Age is a leading risk factor for osteoarthritis, a degenerative joint disease; however, the mechanisms by which degeneration occurs are not well defined. In this issue of Nature Aging, Wang, He, Gong and colleagues report that a specific palmitoyl acyl transferase, ZDHHC11, prevents cartilage degradation by modifying cellular senescence, which highlights its therapeutic potential.

During early brain development, proper cell fate acquisition requires time-sensitive control of gene expression. New work shows that AIRIM variants disrupt cell fate by altering ribosome abundance and the translation of specific mRNAs. The findings pinpoint regulated ribogenesis as a key factor in early human brain development.

Recent literature has explored the contributions of oligodendrocytes and myelin dysfunction to Alzheimer’s disease. Here, we discuss emerging evidence that oligodendrocytes may directly contribute to disease pathology and progression.

Repetitive mechanical forces on the spine cause spinal ligament hypertrophy through an unknown molecular mechanism. We observed in ligaments obtained from patients undergoing surgical spine decompression that force-driven Rho-associated kinase (ROCK) signalling causes accumulation of myofibroblasts from fibroblasts and show that ROCK signalling inhibitors block this force-dependent molecular mechanism contributing to spinal ligament fibrosis.