Table of contents
From the editors
p671 | doi:10.1038/nrm2253
Research Highlights
Development: Bicoid gradient tried and tested | PDF (244 KB)
p673 | doi:10.1038/nrm2248
Networks: The complexity of adhesion | PDF (330 KB)
p674 | doi:10.1038/nrm2237
Meiosis: The telomere bouquet takes control | PDF (121 KB)
p674 | doi:10.1038/nrm2246
Ageing: A new player in the old game | PDF (154 KB)
p675 | doi:10.1038/nrm2250
Cell signalling: A ciliary sensor | PDF (272 KB)
p676 | doi:10.1038/nrm2243
Ageing: Getting old and cancer: hand-in-hand? | PDF (205 KB)
p676 | doi:10.1038/nrm2247
In brief
Ageing | Ageing | Ageing | PDF (116 KB)
p676 | doi:10.1038/nrm2252
In the news
Inadvertent parthenogenesis | PDF (76 KB)
p677 | doi:10.1038/nrm2251
Cell polarity: Acquiring direction from new contacts | PDF (250 KB)
p678 | doi:10.1038/nrm2244
In brief
Cell adhesion | Telomeres | Small RNAs | PDF (96 KB)
p678 | doi:10.1038/nrm2254
Focus on: Ageing
Reviews
Endocrine regulation of ageing
Steven J. Russell & C. Ronald Kahn
p681 | doi:10.1038/nrm2234
Mutations in genes that regulate endocrine signalling pathways can increase the lifespans of worms, flies and mammals. Endocrine pathways might therefore serve as targets for the manipulation of the ageing process and prevention of age-related diseases.
The role of nuclear architecture in genomic instability and ageing
Philipp Oberdoerffer & David A. Sinclair
p692 | doi:10.1038/nrm2238
Changes in nuclear architecture are a hallmark of ageing in yeast and mammals. These changes seem to be driven by DNA damage, which results in age-related alterations in gene expression, and may be a conserved cause of ageing.
Article series: Stem cells
How stem cells age and why this makes us grow old
Norman E. Sharpless & Ronald A. DePinho
p703 | doi:10.1038/nrm2241
Evidence from rodent and human experimental studies supports the view that a decline in the regenerative function of stem cells with age contributes to mammalian ageing and, possibly, several age-associated diseases. However, a few crucial questions remain to be resolved.
Perspectives
Opinion
Cancer and ageing: convergent and divergent mechanisms
Manuel Serrano & Maria A. Blasco
p715 | doi:10.1038/nrm2242
Convergent mechanisms limit the amount of cellular damage and thereby protect against both cancer and ageing, whereas divergent mechanisms prevent excessive proliferation and, therefore, prevent cancer but promote ageing. The net balance between these mechanisms ensures a healthy, cancer-free lifespan until late adulthood in most individuals.
Opinion
Hydrogen peroxide: a metabolic by-product or a common mediator of ageing signals?
Marco Giorgio, Mirella Trinei, Enrica Migliaccio & Pier Giuseppe Pelicci
p722 | doi:10.1038/nrm2240
According to the free-radical theory, oxidizing species — including hydrogen peroxide (H2O2) — are generated during aerobic respiration and cause molecular damage and ageing. However, recent evidence suggests that H2O2 that is produced as a signalling molecule by a selected genetic programme regulates ageing.
Reviews
Cellular senescence: when bad things happen to good cells
Judith Campisi & Fabrizio d'Adda di Fagagna
p729 | doi:10.1038/nrm2233
Various stress signals can induce a state of irreversible cell-cycle arrest that is known as cellular senescence. Understanding the causes of cellular senescence has provided insight into some of its consequences: it is important for suppressing cancer and possibly contributes to ageing.
Self-eating and self-killing: crosstalk between autophagy and apoptosis
M. Chiara Maiuri, Einat Zalckvar, Adi Kimchi & Guido Kroemer
p741 | doi:10.1038/nrm2239
The relationship between autophagy and apoptosis is complex; autophagy constitutes an adaptive stress response that avoids cell death and suppresses apoptosis under certain circumstances, whereas in other cellular settings it contributes to the demise of cells through an alternative cell-death pathway.
