Kumazawa, Xu, Wang and colleagues identify nuclear egress as the mechanism by which cytoplasmic chromatin fragments relocate from the nucleus to the cytoplasm in senescence. They link inflammation to metabolism by showing this egress is regulated by AMPK and metformin.

Using a mouse model with a macrophage-specific DNA repair defect, Niotis, Arvanitaki et al. identify DNA damage-induced autophagy in macrophages as a link from aging to autoimmunity.

Moral-Sanz, Fernández-Carrasco and colleagues identify senolytic properties of sea anemone-derived pore-forming toxins, with selectivity mediated by senescence-associated lipid profiles. An optimized senotoxin improves the efficacy of chemotherapy in mouse models.

Chen et al. identify a brain-to-bone communication axis whereby extracellular vesicles from aged brain neurons transport WDFY1 protein to distal bone, driving bone-fat imbalance and promoting osteoporosis.

LINE-1 retrotransposons are implicated in aging, but their role in cardiac aging specifically is not well understood. Here the authors show that LINE-1 expression rises in mouse hearts with age. Genetic LINE-1 derepression is accompanied by cGAS–STING activation and cardiac dysfunction, while pharmacological inhibition of LINE-1 or STING improves cardiac function in aged mice.

Kumazawa, Xu, Wang and colleagues identify nuclear egress as the mechanism by which cytoplasmic chromatin fragments relocate from the nucleus to the cytoplasm in senescence. They link inflammation to metabolism by showing this egress is regulated by AMPK and metformin.

Using a mouse model with a macrophage-specific DNA repair defect, Niotis, Arvanitaki et al. identify DNA damage-induced autophagy in macrophages as a link from aging to autoimmunity.

Moral-Sanz, Fernández-Carrasco and colleagues identify senolytic properties of sea anemone-derived pore-forming toxins, with selectivity mediated by senescence-associated lipid profiles. An optimized senotoxin improves the efficacy of chemotherapy in mouse models.

Chen et al. identify a brain-to-bone communication axis whereby extracellular vesicles from aged brain neurons transport WDFY1 protein to distal bone, driving bone-fat imbalance and promoting osteoporosis.

Shang, Zhao, Ying and colleagues report that the mechanosensor PIEZO1 senses blood shear stress in hematopoietic stem cells, driving proliferation and myeloid bias. This axis links mechanical force to inflammation-induced aging, and PIEZO1 emerges as a potential therapeutic target.

As we embark on our sixth year of publication, we reflect on what the journal has achieved and highlight some of its successes. This anniversary issue also features two Q&As. One pulls back the curtain on the work of the journal’s backstage team. The other samples the thoughts and opinions of some of the many researchers who supported the journal early on, as authors, advisers or reviewers.

For Nature Aging’s fifth anniversary, we acknowledge the essential work that is done by our colleagues, without which Nature Aging’s monthly publication would not be possible. We speak with some of our internal colleagues about the process of making a journal every month. Rebecca Roberts is a production editor at Springer Nature, Mark McGranaghan is a senior sub editor, Lauren Snape is an art editor and Amanda Karmolinski is a senior editorial assistant. In this Q&A, Rebecca, Mark, Lauren and Amanda pull back the curtain and tell us about the various roles that go into putting it all together.

As Nature Aging celebrates its fifth anniversary, the journal asks some of the researchers who contributed to the journal early on to reflect on the past and the future of aging and age-related disease research, the impact of the field on human health now and in the future, and what challenges need to be addressed to ensure sustained progress.

China’s rapid recent growth has depended on a rural-to-urban migrant workforce that supports its factories, infrastructure and services. As the first generation of these migrants reaches retirement age, life-cycle challenges rooted in institutional exclusion — in particular, through economic disparities in pension support — are becoming apparent and urgently require reform.