bims-caglex Biomed News
on Cellular aging and life extension
Issue of 2026–09–13
two papers selected by
Mario Alexander Guerra Patiño, Universidad Antonio Nariño
  1. Microfluidic Mechanical Reactivation of Senescent Stem Cells.
  2. Characterization of DNA methylation in PBMCs and donor-matched iPSCs shows age-related methylation is reset during stem cell reprogramming.
  1. Small. 2026 Sep 09. e75587
    Microfluidic Mechanical Reactivation of Senescent Stem Cells.
    Soo Bin Jang, Tak-Il Jeon, Geun-Ho Kang, Donghwan Seo, Hyelee Kim, Hancheol Yeo, Jaekwon Seok, Kyung Min Lim, Ahmed Abdal Dayem, Se Jong Kim, Kwonwoo Song, Yeonjoo Kwak, Jeongsoo Hur, Aram J Chung, Ssang-Goo Cho.
      Stem cell aging significantly impairs therapeutic efficacy, requiring innovative strategies to restore potency. We present a microfluidic cell-compressing platform for reactivation (µ-CPR) designed to apply controlled hydrodynamic deformation to late-passage stem cells. This mechanical stimulation facilitates functional reactivation without external chemical cues. Within a defined window, µ-CPR reduces oxidative stress, SA-β-gal activity, and γ-H2A.X foci, while enhancing proliferation and increasing the expression of canonical stemness-associated markers, including OCT4, SOX2, and KLF4. Mechanical stimulation via µ-CPR induces coordinated structural remodeling: nuclei become more compact, actin cortex organization is restored, α-actinin redistributes to focal adhesions, and microtubule networks are restructured, suggesting reorganization of intracellular mechanical architecture. Transcriptomic and proteomic analyses reveal that this process reprograms extracellular matrix remodeling and DNA repair pathways while attenuating pro-fibrotic and senescence-associated secretory phenotype (SASP)-associated pathways. Crucially, this reactivation occurs without compromising fundamental stem cell hallmarks, preserving intrinsic immunophenotypes and multilineage differentiation potential. Functionally, µ-CPR-processed stem cells demonstrate enhanced in vitro wound closure and improved tissue repair in vivo, with efficacy dependent on the applied mechanical dose. This platform establishes a non-genetic, mechanobiological approach to functional stem cell reactivation, offering a scalable strategy for restoring stem cell function and providing a foundation for future cellular rejuvenation strategies.
    Keywords:  cytoskeletal remodeling; mechanobiology; microfluidics; rejuvenation; stem cell reactivation
    DOI:  https://doi.org/10.1002/smll.75587
  2. PLoS One. 2026 ;21(9): e0356501
    Characterization of DNA methylation in PBMCs and donor-matched iPSCs shows age-related methylation is reset during stem cell reprogramming.
    Xylena Reed, Cory A Weller, Sara Saez-Atienzar, Alexandra Beilina, Sultana Solaiman, Makayla Portley, Mary Kaileh, Roshni Roy, Jinhui Ding, A Zenobia Moore, D Thad Whitaker, Bryan J Traynor, Luigi Ferrucci, J Raphael Gibbs, Sonja W Scholz, Mark R Cookson.
      DNA methylation is an important epigenetic mechanism that helps define and maintain cellular functions. It is influenced by many factors, including environmental exposures, genotype, cell type, sex, and aging. Since age is the primary risk factor for developing neurodegenerative diseases, it is important to determine if age-related DNA methylation is retained when cells are reprogrammed to an induced Pluripotent Stem Cell (iPSC) state. Here, we selected peripheral blood mononuclear cells (PBMCs; n = 99) from a cohort of diverse and healthy individuals enrolled in the Genetic and Epigenetic Signatures of Translational Aging Laboratory Testing (GESTALT) study to reprogram to iPSCs. After reprogramming, the resulting iPSCs were evaluated for DNA methylation signatures to determine if they reflect the confounding factors of aging and environmental effects. Data from genome-wide DNA methylation arrays in both cell types showed that age-related methylation measured by epigenetic clocks is largely reset to an early methylation age after reprogramming of PBMCs to iPSCs. We further examined the epigenetic age of each cell type using an Epigenome-wide Association Study (EWAS) and identified a set of methylation Quantitative Trait Loci in each cell type. Our results show that age-related DNA methylation is largely reset in iPSCs, and each cell type has a unique set of methylation sites that are modified by population-level genetic variation.
    DOI:  https://doi.org/10.1371/journal.pone.0356501
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