Recent publications July - September

Read about the publications our colleagues contributed to this quarter

Within the research institutes NUTRIM and CARIM, we study healthy ageing as one of our key research items. Healthy ageing can be understood as the preservation of physiological resilience over time, rather than simply the absence of disease. In a longitudinal cohort of newly-diagnosed colorectal cancer patients, we showed that biomarkers indicative of biological ageing, namely leukocyte telomere length, plasma NAD+ levels and protein carbonyl content, were associated with the development of peripheral neuropathy over two years of follow-up (DOI: 10.1371/journal.pone.0332579). This finding suggests that accelerated ageing phenotypes may increase vulnerability to long-term treatment-related toxicities, highlighting how ageing biology influences survivorship and recovery.

At the cellular and metabolic level, another study demonstrated that deficiency in base excision DNA repair, often seen in ageing populations, leads to increased intracellular lipid accumulation and impaired mitochondrial beta-oxidation in HepG2 cells (DOI: 10.1016/j.dnarep.2025.103880). The implication is that genomic maintenance is critical not just for cancer prevention and longevity, but also for safeguarding metabolic homeostasis and prevention of obesity.

A human in vitro airway model exposed to traffic-derived air pollution (TDAP) in a realistic air–liquid interface set-up induced oxidative stress and inflammatory gene expression, albeit with modest responses and significant donor variability. (DOI: 10.1016/j.envres.2025.122399). This variability may reflect the vulnerability that often comes with ageing. Additionally, human iPSC-derived colon organoids were exposed to the food additive titanium dioxide (E171) and we showed a dose-dependent increases in reactive oxygen species, DNA damage and changes in gene expression. (DOI: 10.1016/j.tiv.2025.106105). Both studies underline that cumulative dietary and airborne exposures may contribute to the “burden” on cellular maintenance systems, thus accelerating biological ageing.

Finally, the vascular involvement in ageing is illustrated by a mouse model of type 1 diabetes, in which overexpression of the glyoxalase-1 enzyme reduced methylglyoxal production and arterial wall stiffening, demonstrating that limiting glycation-related damage can preserve vascular compliance (DOI: 10.1186/s12933-025-02823-4).
 
Integrating these findings, healthy ageing emerges as a process of maintaining genomic and metabolic integrity. It is important to balance oxidative and metabolic stress, reducing cumulative toxic exposures, and safeguarding vascular structure and function.