bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2024–10–27
five papers selected by
Ayesh Seneviratne, McMaster University



  1. NPJ Aging. 2024 Oct 22. 10(1): 47
      Age-related changes in oligodendrocyte precursor cells (OPCs) contribute to white matter dysfunction. In aged mice, we hypothesized that myelin-dense fimbria OPCs possess niche-specific properties, compared to hippocampal OPCs. Aged fimbria OPCs were fewer, larger, and localized to neighboring microglia. We identified age-increased p16/Cdkn2a-expressing OPCs enriched for senescence-related pathways and distinct senescence signatures between hippocampus and fimbria. Aged brain OPC populations differ in microenvironment properties and responses to senescence-directed intervention.
    DOI:  https://doi.org/10.1038/s41514-024-00176-y
  2. Haematologica. 2024 Oct 24.
      Myelodysplastic syndromes (MDS) are a genetically complex and phenotypically diverse set of clonal hematologic neoplasms that occur with increasing frequency with age. MDS has long been associated with systemic inflammatory conditions and disordered inflammatory signaling is implicated in MDS pathogenesis. A rise in sterile inflammation occurs with ageing and the term "inflammaging" has been coined by to describe this phenomenon. This distinct form of sterile inflammation has an unknown role in in the pathogenesis of myeloid malignancies despite shared correlations with age and ageing-related diseases. More recent is a discovery that many cases of MDS arise from clonal hematopoiesis of indeterminate potential (CHIP), an age associated, asymptomatic pre-disease state. The interrelationship between ageing, inflammation and clonal CHIP is complex and likely bidirectional with causality between inflammaging and CHIP potentially instrumental to understanding MDS pathogenesis. Here we review the concept of inflammaging and MDS pathogenesis and explore their causal relationship by introducing a novel framing mechanism of "pre-clonal inflammaging" and "clonal inflammaging". We aim to harmonize research on ageing, inflammation and MDS pathogenesis by contextualizing the current understanding of inflammaging and the ageing hematopoietic system with what is known about the etiology of MDS via its progression from CHIP.
    DOI:  https://doi.org/10.3324/haematol.2023.284944
  3. NPJ Aging. 2024 Oct 24. 10(1): 48
      Senescence and epigenetic alterations stand out as two well-characterized hallmarks of aging. When cells become senescent, they cease proliferation and release inflammatory molecules collectively termed the Senescence-Associated Secretory Phenotype (SASP). Senescence and SASP are implicated in numerous age-related diseases. Senescent cell nuclei undergo epigenetic reprogramming, which intricately regulates SASP expression. This review outlines the current understanding of how senescent cells undergo epigenetic changes and how these alterations govern SASP expression.
    DOI:  https://doi.org/10.1038/s41514-024-00172-2
  4. Clin Sci (Lond). 2024 Nov 06. 138(21): 1343-1356
      It has been recognized for over a century that feeding animals less food than they would normally eat increases lifespan and leads to broad-spectrum improvements in age-related health. A significant number of studies have subsequently shown that restricting total protein, branched chain amino acids or individual amino acids in the diet, as well as ketogenic diets, can elicit similar effects. In addition, it is becoming clear that fasting protocols, such as time-restricted-feeding or every-other-day feeding, without changes in overall energy intake can also profoundly affect rodent longevity and late-life health. In this review, I will provide a historical perspective on various dietary interventions that modulate ageing in rodents and discuss how this understanding of the dietary exposome may help identify future strategies to maintain late-life health and wellbeing in humans.
    Keywords:  Ageing; Aging; Caloric restriction; Dietary restriction; Fasting; Lifespan
    DOI:  https://doi.org/10.1042/CS20241248