bims-cesemi 2026-02-08 papers

Issue of 2026–02–08
six papers selected by
Julio Cesar Cardenas, Universidad Mayor

Cell Metab. 2026 Feb 03. pii: S1550-4131(26)00002-1. [Epub ahead of print]38(2): 254-256

Metastasis gets a little help from immune cell mitochondria.

Michael V Berridge, Renata Zobalova, Jiri Neuzil.

Although a role for mitochondrial transfer has been implicated in metastasis, the mechanisms are unclear. Using mouse metastatic models, Okwan-Duodu and colleagues1 report that mitochondrial transfer from non-cancer immune cells to cancer cells in the tumor facilitates lymph node metastasis via the cGAS/STING immune evasion pathway involving type I interferon.

DOI: https://doi.org/10.1016/j.cmet.2026.01.002

Age Ageing. 2026 Feb 01. pii: afag022. [Epub ahead of print]55(2):

Association of mitochondrial oxidative capacity with physical fitness in ageing: the Baltimore longitudinal study of ageing.

Caterina Trevisan, Qu Tian, Kenneth W Fishbein, Sarah Church, Eleanor M Simonsick, Josephine M Egan, Stefano Volpato, Luigi Ferrucci.

BACKGROUND: In younger individuals, fitness is mostly influenced by muscle mitochondrial oxidative phosphorylation (OxPhos) and cardiac output. However, compared with younger individuals, various impairments may also negatively affect fitness in older adults.
OBJECTIVE: To investigate the relationship of OxPhos with cardiorespiratory fitness, the energetic cost of walking and aerobic resilience with respect to age.
DESIGN: Cross-sectional.
SETTING: Population.
SUBJECTS: Six hundred and forty-nine Baltimore longitudinal study of ageing participants (mean age 64.5 years, 56.9% females).
METHODS: Muscle mitochondrial OxPhos was measured as phosphocreatine recovery rate (kPCr) through 31P magnetic resonance spectroscopy. Based on age- and sex-specific kPCr z-scores, we classified individuals with low (≤ -0.5 standard deviations [SD]), average (-0.5 to 0.5SD) and high (>0.5SD) OxPhos. Cardiorespiratory fitness was measured as peak oxygen consumption (MVO2 peak) during a treadmill testing. The energetic cost of usual pace walking was expressed as the average oxygen consumption per 100 metres. Aerobic resilience was the ratio between MVO2 peak and average VO2 during usual pace walking.
RESULTS: Participants with higher kPCr had 4.07 (95%CI: 2.88, 5.26) ml/kg/min higher MVO2 peak and 0.19 (95%CI: 0.06, 0.32) higher aerobic resilience than those with lower kPCr. The energetic cost of walking was greater by 0.84 (95% CI: 0.21, 1.47) ml/kg/100 m in those with high than low kPCr. A multiplicative interaction between age and kPCr was identified in the regressions predicting MVO2 peak and aerobic resilience (pinteraction = 0.01), with differences between OxPhos groups attenuating after age 70.
CONCLUSION: Muscle mitochondrial OxPhos contributes to interindividual variability in cardiorespiratory fitness, especially in young and middle adulthood.

Keywords: ageing; cohort study; energetic cost of walking; mitochondria; older people; physical fitness

DOI: https://doi.org/10.1093/ageing/afag022

Nature. 2026 Feb 05.

These mysterious ridges could be the secret to younger skin.

Nick Petrić Howe.

Keywords: Cell biology; Health care; Stem cells

DOI: https://doi.org/10.1038/d41586-026-00364-8

bioRxiv. 2026 Jan 14. pii: 2026.01.13.699119. [Epub ahead of print]

Vitamin B12 Improves Skeletal Muscle Mitochondrial Biology in Aged Mice.

Abigail R Williamson, Angad Yadav, Wenxia Ma, Susan Schmitt, Shelby Rorrer, Lauren E Odom, Luisa F Castillo, Chloe T Purello, Olga V Malysheva, James Mobley, Martha Field, Anna E Thalacker-Mercer.

Age-related skeletal muscle deterioration is a commonly reported disability among older adults, attributed to several factors including mitochondrial dysfunction, a major hallmark of aging. Therapies to attenuate or reverse mitochondrial decline are limited. Despite identified positive relationships between vitamin B12 (B12) and mitochondrial biology, the impact of B12 supplementation on skeletal muscle mitochondria, in advanced aged, has not been examined. Thus, the impact of B12 supplementation on skeletal muscle mitochondrial biology was examined in (i) aged female mice, given 12 weeks of B12 supplementation (SUPP) or vehicle control, and (ii) in human primary myotubes. In the mouse model, mitochondrial DNA and content were measured with PCR and citrate synthase activity, respectively; mitochondrial morphology was examined using transmission electron microscopy; mitochondrial function was examined using extracellular metabolic flux analysis; and proteins and pathway enrichment was identified with proteomics. In the cell model, ROS and glutathione was measured using luminescent assays. The results demonstrated that SUPP in aged mice increased muscle mitochondrial content and improved morphology. Further, differentially expressed proteins were enriched in TCA cycle, OXPHOS, and oxidative stress pathways. In the cell model, B12 supplementation reduced ROS levels. This is the first study, to our knowledge, examining the impact of B12 supplementation on skeletal muscle mitochondrial biology in aged female mice. Results suggest that B12 supplementation improves mitochondrial biology in aged female mice.

DOI: https://doi.org/10.64898/2026.01.13.699119

Nat Cell Biol. 2026 Feb 02.

ER remodelling is a feature of ageing and depends on ER-phagy.

Eric K F Donahue, Nathaniel L Hepowit, Elizabeth M Ruark, Alexandra G Mulligan, Brennen Keuchel, Nicholas D Urban, Li Peng, Stedman Stephens, Derek J Johnson, Natalie S Wallace, Lauren P Jackson, Mark H Ellisman, Rafael Arrojo E Drigo, Andrew W Folkmann, Matthias C Truttmann, Jason A MacGurn, Kristopher Burkewitz.

The endoplasmic reticulum (ER) comprises an array of subdomains, each defined by a characteristic structure and function. Although altered ER processes are linked to age-onset pathogenesis, it is unclear whether shifts in ER structure or dynamics underlie these functional changes. Here we establish ER structural and functional remodelling as a conserved feature of ageing across yeast, Caenorhabditis elegans and mammals. Focusing on C. elegans as the exemplar of metazoan ageing, we reveal striking age-related reductions in ER volume across diverse tissues and a morphological shift from rough sheets to tubular ER. This morphological transition corresponds with large-scale shifts in ER proteome composition from protein synthesis to lipid metabolism, a phenomenon conserved in mammalian tissues. We show that Atg8 and ULK1-dependent ER-phagy drives age-associated ER remodelling through tissue-specific factors, including the previously uncharacterized ER-phagy regulator TMEM-131 and the IRE-1-XBP-1 branch of the unfolded protein response. Providing support for a model where ER remodelling is adaptive, diverse lifespan-extending paradigms downscale and remodel ER morphology throughout life. Furthermore, mTOR-dependent lifespan extension in yeast and worms requires ER-phagy, indicating that ER remodelling is a proactive and protective response during ageing. These results reveal ER-phagy and ER dynamics as pronounced, underappreciated mechanisms of both normal ageing and age-delaying interventions.

DOI: https://doi.org/10.1038/s41556-025-01860-1