bims-cesemi Biomed News
on Cellular senescence and mitochondria
Issue of 2025–11–09
fourteen papers selected by
Julio Cesar Cardenas, Universidad Mayor
  1. Modulation of Inositol 1,4,5-Trisphosphate Receptors by Their Primary Physiological Ligands, IP3, Ca2+, and ATP.
  2. Direct measurements of luminal Ca2+ with endo-lysosomal GFP-aequorin reveal functional IP3 receptors.
  3. Adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly.
  4. Coordinated Remodeling of Ca2+ Signaling and Intracellular Organelles During Cell Division.
  5. Defining Microbiota-Derived Metabolite Butyrate as a Senomorphic: Therapeutic Potential in the Age-Related T Cell Senescence.
  6. The ER thioredoxin-related transmembrane protein TMX2 controls redox-mediated tethering of ER-mitochondria contacts.
  7. NAD depletion in skeletal muscle does not compromise muscle function or accelerate aging.
  8. The impact of ageing and frailty on wound healing.
  9. Senolytic-sensitive p16Ink4a+ fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity.
  10. Cell-type-specific dysregulation of mitochondrial calcium signaling in Alzheimer's disease.
  11. Targeting cancer glutamine dependency with a first-in-class inhibitor of the mitochondrial glutamine transporter SLC1A5_var.
  12. SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.
  13. Open problems in ageing science: a roadmap for biogerontology.
  14. Cell populations in human breast cancers are molecularly and biologically distinct with age.
  1. Cold Spring Harb Perspect Biol. 2025 Nov 03. pii: a041762. [Epub ahead of print]
    Modulation of Inositol 1,4,5-Trisphosphate Receptors by Their Primary Physiological Ligands, IP3, Ca2+, and ATP.
    Vikas Arige, Xiaoxuan Lin, David M MacLean, Irina I Serysheva, David I Yule.
      Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are ubiquitously expressed intracellular calcium (Ca2+) release channels predominantly localized to the endoplasmic reticulum. There are three IP3R subtypes, which assemble as homo-/heterotetramers. The opening of IP3Rs requires binding of one IP3 per monomer and Ca2+ Recent high-resolution cryogenic electron microscopy (cryo-EM) structures of IP3Rs in combination with functional assays have greatly increased our understanding of the structural basis for IP3R channel opening and closing. IP3R channel activation is facilitated by IP3 and Ca2+ binding to the activation site. Channel inactivation occurs in the presence of IP3 and high Ca2+ when Ca2+ is bound to the low-affinity Ca2+-binding motif. Specifically, in the near atomic resolution structures of IP3Rs, densities corresponding to the primary agonists-IP3 and Ca2+-and the allosteric modulator adenosine triphosphate (ATP) were identified. In this article, we aim to provide a comprehensive overview of the current understanding of structure-function relationships for IP3Rs mediated by IP3, Ca2+, and ATP.
    DOI:  https://doi.org/10.1101/cshperspect.a041762
  2. J Cell Biol. 2025 Dec 01. pii: e202410094. [Epub ahead of print]224(12):
    Direct measurements of luminal Ca2+ with endo-lysosomal GFP-aequorin reveal functional IP3 receptors.
    Belén Calvo, Patricia Torres-Vidal, Alba Delrio-Lorenzo, Carla Rodriguez, Francisco J Aulestia, Jonathan Rojo-Ruiz, Beatriz Callejo, Bridget M McVeigh, Marco Keller, Christian Grimm, Viola Oorschot, Vera Moiseenkova-Bell, David I Yule, Javier Garcia-Sancho, Sandip Patel, M Teresa Alonso.
      Endo-lysosomes are considered acidic Ca2+ stores, but direct measurements of luminal Ca2+ within them are limited. Here, we report that the Ca2+-sensitive luminescent protein aequorin does not reconstitute with its cofactor at highly acidic pH but that a significant fraction of the probe is functional within a mildly acidic compartment when targeted to the endo-lysosomal system. We leveraged this probe (ELGA) to report Ca2+ dynamics in this compartment. We show that Ca2+ uptake is ATP-dependent and sensitive to blockers of ER Ca2+ pumps. We find that the Ca2+ mobilizing messenger IP3 evokes robust luminal responses in wild-type cells, but not in IP3R knockout cells. Responses were comparable to those evoked by activation of the endo-lysosomal ion channels TPCs and TRPMLs. Stimulation with IP3-forming agonists also mobilized the store in intact cells. Super-resolution microscopy analysis was consistent with the presence of IP3Rs within the endo-lysosomal system. Our data reveal a physiologically relevant, IP3-sensitive store of Ca2+ within the endo-lysosomal system.
    DOI:  https://doi.org/10.1083/jcb.202410094
  3. Cell Death Differ. 2025 Nov 01.
    Adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly.
    Jose C Casas-Martinez, Qin Xia, Penglin Li, Maria Borja-Gonzalez, Antonio Miranda-Vizuete, Emma McDermott, Peter Dockery, Leo R Quinlan, Katarzyna Goljanek-Whysall, Afshin Samali, Brian McDonagh.
      The transfer of information and metabolites between the mitochondria and the endoplasmic reticulum (ER) is mediated by mitochondria-ER contact sites (MERCS), allowing adaptations in response to changes in cellular homeostasis. MERCS are dynamic structures essential for maintaining cell homeostasis through the modulation of calcium transfer, redox signalling, lipid transfer, autophagy and mitochondrial dynamics. Under stress conditions such as ER protein misfolding, the Unfolded Protein Response (UPRER) mediates PERK and IRE1 activation, both of which localise at MERCS. Adaptive UPRER signalling enhances mitochondrial function and calcium import, whereas maladaptive responses lead to excessive calcium influx and apoptosis. In this study, induction of mild acute ER stress with tunicamycin (TM) in myoblasts promoted myogenesis that required PERK for increased MERCS assembly, mitochondrial turnover and function. Similarly, treatment of C. elegans embryos with an acute low concentration of TM, promoted an extension in lifespan and health-span. The adaptive ER stress response following a low dose of TM in both myoblasts and C. elegans, increased MERCS assembly and activated autophagy machinery, ultimately promoting an increase in mitochondrial remodelling. However, these beneficial adaptations were dependent on the developmental stage, as treatment of myotubes or adult C. elegans resulted in a maladaptive response. In both models the adaptations to UPRER activation were dependent on PERK signalling and its interaction with the UPRmt. The results demonstrate PERK is required for the increased mitochondrial ER communication in response to adaptive UPR signalling, promoting mitochondrial remodelling and improved physiological function.
    DOI:  https://doi.org/10.1038/s41418-025-01603-7
  4. Annu Rev Physiol. 2025 Nov 07.
    Coordinated Remodeling of Ca2+ Signaling and Intracellular Organelles During Cell Division.
    Fang Yu, Lama Assaf, Khaled Machaca.
      Cell division is essential for organismal growth and development and is associated with changes in signaling dynamics, including Ca2+ signaling, to meet structural, functional, and energetic needs. The process of cell division must ensure equal separation of both the genetic material and cellular organelles. Organelle segregation to the daughter cells is in most cases associated with their remodeling to support equal distribution. Here, we review the concurrent remodeling of organelles and Ca2+ signaling during cell division. Interesting patterns emerge, showing that organelle dynamics, specifically the plasma membrane, endoplasmic reticulum, and mitochondria, underlie Ca2+ signaling remodeling during cell division.
    DOI:  https://doi.org/10.1146/annurev-physiol-061324-091825
  5. Aging Cell. 2025 Nov 07. e70257
    Defining Microbiota-Derived Metabolite Butyrate as a Senomorphic: Therapeutic Potential in the Age-Related T Cell Senescence.
    Nia Paddison Rees, Jessica Conway, Ben Dugan, Sayeda S Amir, Aimee Parker, Simon R Carding, Niharika A Duggal.
      Advancing age is accompanied by an accumulation of senescent T cells that secrete pro-inflammatory senescence-associated secretory phenotype (SASP) molecules. Gut-microbiota-derived signals are increasingly recognised as immunomodulators. In the current study, we demonstrated that ageing and the accumulation of senescent T cells are accompanied by a reduction in microbial-derived short-chain fatty acids (SCFAs). Culturing aged T cells in the presence of butyrate suppresses the induction of a senescence phenotype and inhibits the secretion of pro-inflammatory SASP factors, such as IL6 and IL8. Administration of faecal supernatants from young mice rich in butyrate prevented in vivo accumulation of senescent spleen cells in aged mice. The molecular pathways governing butyrate's senomorphic potential include a reduced expression of DNA damage markers, lower mitochondrial ROS accumulation, and downregulation of mTOR activation, which negatively regulates the transcription factor NFκB. Our findings establish butyrate as a potent senomorphic agent and provide the evidence base for future microbiome restitution intervention trials using butyrate supplements for combating T cell senescence, ultimately reducing inflammation and combating age-related pathologies to extend lifelong health.
    Keywords:  T cell; ageing; cellular senescence; inflammation
    DOI:  https://doi.org/10.1111/acel.70257
  6. Cell Rep. 2025 Oct 30. pii: S2211-1247(25)01257-4. [Epub ahead of print]44(11): 116486
    The ER thioredoxin-related transmembrane protein TMX2 controls redox-mediated tethering of ER-mitochondria contacts.
    Junsheng Chen, Megan C Yap, Arthur Bassot, Danielle M Pascual, Tadashi Makio, Jannik Zimmermann, Heather Mast, Rakesh Bhat, Samuel G Fleury, Yuxiang Fan, Adriana Zardini Buzatto, Jack Moore, Klaus Ballanyi, Liang Li, Michael Overduin, M Joanne Lemieux, Hélène Lemieux, Grazia M S Mancini, Bruce Morgan, Paul C Marcogliese, Thomas Simmen.
      Thioredoxin-related transmembrane proteins (TMXs) of the endoplasmic reticulum (ER) determine not only redox conditions within the ER lumen but also the formation and function of ER-mitochondria membrane contact sites (ERMCS). The presence of cytosolic, reactive oxygen species (ROS)-derived redox nanodomains at ERMCS suggests TMXs could also control these. The prime candidate for such a function is TMX2, the sole TMX family protein with a cytosolic thioredoxin domain. Indeed, TMX2 controls the extent of ERMCS through interaction with outer mitochondrial membrane proteins, including TOM70. Assisted by cytosolic peroxiredoxins, TMX2 moderates the sulfenylation of the TOM70 C206 residue. Thereby, TMX2 reduces mitochondrial Ca2+ uptake and metabolism. Accordingly, mutation of the TMX2 gene in cells from a patient with a neurodevelopmental disorder with microcephaly, cortical malformations, and spasticity (NEDMCMS) results in hyperactive mitochondria. In a fly in vivo NEDMCMS model, TMX2 knockdown manifests predominantly in glial cells, where it prevents seizure-like behavior.
    Keywords:  CP: Molecular biology; Ca(2+); ER; MCS; PRDX; TMX2; TOM70; endoplasmic reticulum; membrane contact sites; mitochondria; peroxiredoxin; redox
    DOI:  https://doi.org/10.1016/j.celrep.2025.116486
  7. Cell Metab. 2025 Nov 04. pii: S1550-4131(25)00480-2. [Epub ahead of print]
    NAD depletion in skeletal muscle does not compromise muscle function or accelerate aging.
    Sabina Chubanava, Iuliia Karavaeva, Amy M Ehrlich, Roger M Justicia, Astrid L Basse, Ivan Kulik, Emilie Dalbram, Danial Ahwazi, Samuel R Heaselgrave, Kajetan Trošt, Ben Stocks, Ondřej Hodek, Raissa N Rodrigues, Jesper F Havelund, Farina L Schlabs, Steen Larsen, Caio Y Yonamine, Carlos Henriquez-Olguín, Daniela Giustarini, Ranieri Rossi, Zachary Gerhart-Hines, Thomas Moritz, Juleen R Zierath, Kei Sakamoto, Thomas E Jensen, Nils J Færgeman, Gareth G Lavery, Atul S Deshmukh, Jonas T Treebak.
      
    DOI:  https://doi.org/10.1016/j.cmet.2025.10.020
  8. Br J Nurs. 2025 Nov 06. 34(20): S27-S34
    The impact of ageing and frailty on wound healing.
    Fiona Chalk, Annette Palmer.
      As the global population ages, the prevalence of complex wounds and delayed healing is becoming a significant concern. Ageing leads to physiological changes such as reduced skin elasticity, weakened immune responses and slower cellular regeneration, all of which delay wound healing. Frailty, marked by reduced physiological reserves and heightened vulnerability to stressors, worsens these issues. Together, ageing and frailty increase the risk of tissue breakdown, infection rates, prolonged healing times and rising healthcare costs. This article examines the relationship between ageing, frailty, increased risk of wounds and wound healing, drawing on recent research to highlight key challenges. It also provides evidence-based recommendations for practice, highlighting the importance of preventive strategies and holistic wound assessment. The findings emphasise the importance of a proactive approach to improve clinical outcomes in older, frail populations while ensuring efficient use of healthcare resources.
    Keywords:  Ageing; Chronic; Frailty; Hard-to-heal; Non-healing; Skin integrity; Wound healing; Wounds
    DOI:  https://doi.org/10.12968/bjon.2025.0023
  9. Cell Stem Cell. 2025 Nov 03. pii: S1934-5909(25)00373-X. [Epub ahead of print]
    Senolytic-sensitive p16Ink4a+ fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity.
    Jin Young Lee, Nabora Reyes, Sang-Ho Woo, Nancy C Allen, Tsukasa Kadota, Andrew Lechner, Ritusree Biswas, Sakshi Goel, Fia Stratton, Chaoyuan Kuang, Tatsuya Tsukui, Vincent Auyeung, Aaron S Mansfield, Lindsay M LaFave, Tien Peng.
      Senescence has been demonstrated to either inhibit or promote tumorigenesis. Resolving this paradox requires spatial mapping and functional characterization of senescent cells in the native tumor niche. Here, we identify p16Ink4a+ cancer-associated fibroblasts enriched with senescent phenotypes that promote fatty acid uptake and utilization by aggressive lung adenocarcinoma (LUAD) driven by Kras and p53 mutations. Furthermore, rewiring of lung cancer metabolism by p16Ink4a+ cancer-associated fibroblasts also alters tumor cell identity to a highly plastic/dedifferentiated state associated with progression in murine and human LUAD. Our ex vivo senolytic screening platform identifies XL888, an HSP90 inhibitor, that clears p16Ink4a+ cancer-associated fibroblasts in vivo. XL888 administration after establishment of advanced LUAD significantly reduces tumor burden concurrent with the loss of plastic tumor cells. Our study identifies a druggable component of the tumor stroma that fulfills the metabolic requirement of tumor cells to acquire a more aggressive phenotype.
    Keywords:  cancer-associated fibroblasts; lung adenocarcinoma; p16(INK4a); senescence; senolytics; spatial transcriptomics; tumor cell plasticity; tumor metabolism; tumor microenvironment
    DOI:  https://doi.org/10.1016/j.stem.2025.10.005
  10. Cell Commun Signal. 2025 Nov 03. 23(1): 472
    Cell-type-specific dysregulation of mitochondrial calcium signaling in Alzheimer's disease.
    Shatakshi Shukla, Ashlesha A Kadam, Shanikumar Goyani, Natasha Jaiswal, Kunal Samantaray, Shiridhar Kashyap, Dhanendra Tomar, Pooja Jadiya.
       BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid plaques, tau tangles, and synaptic dysfunction. Despite decades of research, effective disease-modifying therapies remain elusive, highlighting the need for alternative therapeutic targets. While neurons have traditionally been the focus of AD studies, increasing evidence underscores critical roles for glial cells particularly microglia and astrocytes in disease progression. Mitochondrial calcium (mCa2+) dysregulation has emerged as a key contributor to neurodegeneration, yet how mCa2⁺ signaling varies across brain cell types and contributes to AD pathology remains poorly understood.
    METHODS: We developed stable human SH-SY5Y (neuroblastoma-derived cells), HMC3 (microglial-like cells), and SVGp12 (astrocytic-like cells) immortalized cell lines expressing APP mutations (Swedish, Florida, and London; APPswe/F/L). We assessed mitochondrial calcium uniporter (mtCU) expression, mCa2+ flux using ratiometric calcium (Ca2+) indicators, and evaluated calcium retention capacity (mito-CRC) as a readout of mitochondrial permeability transition pore opening. Bioenergetic parameters including ATP, NADH, membrane potential, and oxygen consumption rate (OCR) were measured alongside structural mitochondrial changes, ROS levels, and cell death using imaging and biochemical assays.
    RESULTS: APPswe/F/L expression induced mitochondrial dysfunction across all brain immortalized cell types, with neuroblastoma-derived cells exhibiting the highest susceptibility to mCa2+ overload, energy failure, and cell death. Compared to neuroblastoma-derived cells, glial-like cells (astrocytic-like and microglial-like cells) showed higher expression of mtCU components, elevated mCa2+ uptake at high Ca²⁺ concentrations, and greater mito-CRC. Conversely, neuroblastoma-derived cells displayed faster mCa2+ uptake at low Ca2+ levels, indicating distinct regulatory thresholds. Glial-like cells exhibited more elaborate mitochondrial networks and enhanced metabolic capacity, yet all cell types showed impaired mitochondrial structure, reduced membrane potential and respiration, and increased ROS under mutant APP expression.
    CONCLUSIONS: This study reveals cell-type-specific differences in mCa2+ signaling and mitochondrial function in AD, uncovering unique vulnerabilities in neuroblastoma-derived and glial-like cells. These findings highlight the need for cell-targeted strategies to restore mCa2+ homeostasis and mitochondrial function in AD.
    Keywords:  Alzheimer’s disease; Cell death; Cell-type specificity; Glial-like cells; Mitochondrial bioenergetics; Mitochondrial calcium; Neuroblastoma-derived cells; Oxidative stress
    DOI:  https://doi.org/10.1186/s12964-025-02460-0
  11. Nat Commun. 2025 Nov 03. 16(1): 9690
    Targeting cancer glutamine dependency with a first-in-class inhibitor of the mitochondrial glutamine transporter SLC1A5_var.
    Yulseung Sung, Ya Chun Yu, Mirim Lee, Seonghun Lim, Yechan Lee, Mincheol Kang, Doru Kwon, Apeksha Parajulee, Junjeong Choi, Do Sik Min, Kuglae Kim, Wan Namkung, Yun-Hee Kim, Sang Myung Woo, Nam Doo Kim, Hee Chan Yoo, Jung Min Han.
      The mitochondrial glutamine transporter SLC1A5_var plays a central role in the metabolic reprogramming of cancer cells by facilitating glutamine import into mitochondria for energy production and redox homeostasis. Despite its critical function, the development of effective and selective inhibitors targeting SLC1A5_var has remained a significant challenge. Here, we introduce iMQT_020, a selective allosteric inhibitor identified through structure-based screening. iMQT_020 disrupts the trimeric assembly of SLC1A5_var, causing metabolic crisis in cancer cells and selectively suppressing their growth. Mechanistically, iMQT_020 reduces glutamine anaplerosis and oxidative phosphorylation, resulting in a broad disruption of cancer metabolism. Additionally, iMQT_020 treatment epigenetically upregulates PD-L1 expression, enhancing the efficacy of combination therapies with anti-PD-L1 immune checkpoint inhibitors. These findings highlight the therapeutic potential of targeting SLC1A5_var as a critical metabolic vulnerability in cancer and demonstrate that targeting allosteric interprotomer interactions is a novel and promising therapeutic strategy for cancer treatment.
    DOI:  https://doi.org/10.1038/s41467-025-64730-2
  12. Aging (Albany NY). 2025 Oct 30. 17
    SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.
    Ryan Wallis, Bethany K Hughes, Madeleine Moore, Emily A O'Sullivan, Luke C McIlvenna, Luke Gammon, Anthony Hope, Fiona Bellany, Parul Dixit, Claire Mackenzie, Charlotte Green, David Gray, Cleo L Bishop.
       BACKGROUND: Senescence identification is rendered challenging due to a lack of universally available biomarkers. This represents a bottleneck in efforts to develop pro-senescence therapeutics - agents designed to induce the arrest of cellular proliferation associated with a senescence response in cancer cells for therapeutic gain. This is particularly true in contexts such as basal-like breast cancer (BLBC), which often express high levels of widely reported senescence hallmarks, which has led to the designation of these subtypes as senescence marker positive (Sen-Mark+). Unfortunately, these are often cancers with the most limited treatment options, where novel pro-senescence compounds would be of potential clinical utility.
    RESULTS: To address these challenges, we have developed SAMP-Score, a machine learning classification tool for identifying senescence induction in Sen-Mark+ cancers. This technique builds upon our previous observation that senescent cells develop distinct senescence-associated morphological profiles (SAMPs), which can be assessed readily in traditionally challenging contexts for senescence identification, including high-throughput screens.
    CONCLUSIONS: Through application of SAMP-Score, we have identified QM5928, a novel pro-senescence compound, that is able to induce senescence in a variety of Sen-Mark+ cancers and has potential utility as a tool molecule to explore the mechanisms and pathways through which senescence induction occurs in these cells.
    Keywords:  SAMP-Score; Sen-Mark+; high-throughput compound screening; machine learning; pro-senescence; senescence; senescent marker positive cancer cells
    DOI:  https://doi.org/10.18632/aging.206333
  13. Geroscience. 2025 Nov 08.
    Open problems in ageing science: a roadmap for biogerontology.
    Angelo Talay, Aleksey V Belikov, Paul Ka Po To, Hamid H Alfatemi, Uri Alon, Joris Deelen, Collin Y Ewald, David Gems, Vera Gorbunova, Jan Gruber, Sara Hägg, John Hemming, Steve Horvath, Alaattin Kaya, Caitlin J Lewis, Andrea B Maier, Maria B Marinova, Graham Pawelec, Shahaf Peleg, Suresh Rattan, Morten Scheibye-Knudsen, Tomas Schmauck-Medina, Vardan Saroyan, Andrei Seluanov, Alexandra Stolzing, Emma Teeling, Robert W Williams, Todd White, Maximilian Unfried, João Pedro de Magalhães.
      The field of ageing science has gone through remarkable progress in recent decades, yet many fundamental questions remain unanswered or unexplored. Here we present a curated list of 100 open problems in ageing and longevity science. These questions were collected through community engagement and further analysed using Natural Language Processing to assess their prevalence in the literature and to identify both well-established and emerging research gaps. The final list is categorised into different topics, including molecular and cellular mechanisms of ageing, comparative biology and the use of model organisms, biomarkers and the development of therapeutic interventions. Both long-standing questions and more recent and specific questions are featured. Our comprehensive compilation is available to the biogerontology community on our website ( www.longevityknowledge.app ). Overall, this work highlights current key research questions in ageing biology and offers a roadmap for fostering future progress in biogerontology.
    Keywords:  Ageing and longevity science; Biogerontology; Biology of ageing; Database; Natural language processing
    DOI:  https://doi.org/10.1007/s11357-025-01964-4
  14. Nat Aging. 2025 Nov 04.
    Cell populations in human breast cancers are molecularly and biologically distinct with age.
    Adrienne Parsons, Esther Sauras Colón, Meghana Manjunath, Hanyun Zhang, Julia Chen, Milos Spasic, Beyza Koca, Busem Binboga Kurt, Rachel A Freedman, Elizabeth A Mittendorf, Alexander Swarbrick, Peter van Galen, Sandra S McAllister.
      Aging is associated with increased breast cancer risk, and the oldest and youngest patients have worse outcomes, irrespective of subtype. It is unknown how age affects cells in the breast tumor microenvironment or how they contribute to age-related pathology. Here we discover age-associated differences in cell states in human estrogen receptor-positive and triple-negative breast cancers using analyses of existing bulk and single-cell transcriptomic data. We generate and apply an Age-Specific Program ENrichment (ASPEN) analysis pipeline, revealing age-related changes, including increased tumor cell epithelial-mesenchymal transition and cancer-associated fibroblast inflammatory responses in triple-negative breast cancer. Estrogen receptor-positive breast cancer displays increased ESR1 expression and reduced vascular and immune cell metabolism with age. Cell interactome analysis reveals candidate signaling pathways that drive age-related cell states. Spatial analyses across independent clinical cohorts support the computational findings. This work identifies potential targets for age-adapted therapeutic interventions for breast cancer.
    DOI:  https://doi.org/10.1038/s43587-025-00984-1
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