bims-nimamd Biomed News
on Neuroimmunity and neuroinflammation in ageing and metabolic disease
Issue of 2025–07–20
25 papers selected by
Fawaz Alzaïd, Sorbonne Université



  1. Nature. 2025 Jul 16.
      
    Keywords:  Cardiovascular biology; Medical research; Microbiome
    DOI:  https://doi.org/10.1038/d41586-025-02060-5
  2. Nat Aging. 2025 Jul 14.
      Growing evidence suggests that the induction of cellular senescence in vascular cells is causally linked to the etiology of cardiovascular diseases. To investigate systematically the heterogeneity of senescent vascular cells in atherosclerosis, we used a high-fat diet and PCSK9 overexpression to induce atherosclerosis in a senescence reporter mouse model (p16-tdTomato+/-) and performed single-cell RNA sequencing on whole aortas. Using the SenMayo and CellAge gene sets, we identified four clusters of vascular smooth muscle cells (VSMCs), fibroblasts and T cells enriched in features of senescence, which were reduced upon treatment with the senolytic agent ABT-737. We then derived a global senescence signature of atherosclerosis including Spp1, Ctsb and Tnfrsf11b mRNAs. We validated the enrichment of these mRNAs in senescence by using spatial transcriptomics in a second mouse model of atherosclerosis and senolysis (Ldlr-/-; p16-3MR), as well as by analyzing in vitro models of human VSMC senescence. Our results uncover a vascular-specific transcriptomic signature of senescence that may be exploited for tracking and treating age-related vascular diseases.
    DOI:  https://doi.org/10.1038/s43587-025-00889-z
  3. Nat Aging. 2025 Jul;5(7): 1181-1185
    Global Neurodegeneration Proteomics Consortium (GNPC) Scientific Steering Committee
      
    DOI:  https://doi.org/10.1038/s43587-025-00920-3
  4. Nat Neurosci. 2025 Jul 14.
      Microglial spatial heterogeneity remains a crucial yet not fully answered question in the context of potential cell-directed therapies for Alzheimer's disease (AD). There is an unclear understanding of the dynamics of distinct microglia states adjacent to or far from amyloid-beta (Aβ) plaques and their contributions to neurodegenerative diseases. Here we combine multicolor fluorescence cell fate mapping, single-cell transcriptional analysis, epigenetic profiling, immunohistochemistry and computational modeling to comprehensively characterize the relation of plaque-associated microglia (PAM) and non-plaque-associated microglia (non-PAM) in a mouse model of AD. We show that non-PAM are a distinct and highly dynamic microglial state, transitioning to PAM after Aβ plaque deposition in female mice. Non-PAM modulate the cell population expansion in response to amyloid deposition and rapidly respond to environmental cues. Indeed, Csf1 signaling modulates non-PAM-to-PAM transition during disease progression. Our data suggest that microglia states and their dynamics between each other can have distinct contributions to disease, and they may be targeted for the treatment of AD.
    DOI:  https://doi.org/10.1038/s41593-025-02006-0
  5. Nat Biotechnol. 2025 Jul;43(7): 1053
      
    DOI:  https://doi.org/10.1038/s41587-025-02728-3
  6. Mol Metab. 2025 Jul 15. pii: S2212-8778(25)00115-2. [Epub ahead of print] 102208
      TCF7L2 harbors the strongest genetic association with diabetes identified thus far. However, its function in liver has remained unclear. Here, we find that liver-specific deletion Tcf7l2 has little effect on plasma glucose, but disrupts hepatic zonation. That is, in the normal liver, many genes show gradients of expression across the liver lobule; in the absence of Tcf7l2, these gradients collapse. One major consequence is the disorganization of glutamine metabolism, with a loss of the glutamine production program, ectopic expression of the glutamine consumption program, and a decrease in glutamine levels. In parallel, metabolomic profiling shows glutamine to be the most significantly decreased metabolite in the plasma of individuals harboring the rs7903146 variant in TCF7L2. Taken together, these data indicate that hepatic TCF7L2 has a secondary role in glycemic control, but a primary role in maintaining transcriptional architecture and glutamine homeostasis.
    Keywords:  Zonation; diabetes; metabolism; transcription
    DOI:  https://doi.org/10.1016/j.molmet.2025.102208
  7. Nat Cell Biol. 2025 Jul 15.
      Metabolic cues are crucial for regulating haematopoietic stem and progenitor cells (HSPCs). However, the metabolic profile of human HSPCs remains poorly understood due to the limited number of cells and the scarcity of bone marrow samples. Here we present the integrated metabolome, lipidome and transcriptome of human adult HSPCs (lineage-, CD34+, CD38-) upon differentiation, ageing and acute myeloid leukaemia. The combination of low-input targeted metabolomics with our newly optimized low-input untargeted lipidomics workflow allows us to detect up to 193 metabolites and lipids from a starting material of 3,000 and 5,000 HSPCs, respectively. Among other findings, we observe elevated levels of the essential nutrient choline in HSPCs compared with downstream progenitors, which decline upon ageing and further decrease in acute myeloid leukaemia. Functionally, we show that choline supplementation fuels lipid production in HSPCs and enhances stemness. Overall, our study provides a comprehensive resource identifying metabolic changes that can be utilized to promote and enhance human stem cell function.
    DOI:  https://doi.org/10.1038/s41556-025-01709-7
  8. Nat Commun. 2025 Jul 17. 16(1): 6574
      Immature neutrophils (imNeu) are a minor population of circulating neutrophils that migrate from the bone marrow (BM) into the circulation and inflamed tissues during infection, injury, physical stress, and cancer. However, the underlying mechanism of their mobilization from BM and its pathophysiological significance remains incompletely understood. Here, we show that interferon-gamma (IFN-γ) derived from type 1 innate lymphoid cells (ILC1) enhances the migration of imNeu, but not mature neutrophils, from the BM into inflamed liver tissue with ischemia-reperfusion injury and the blood circulation during polymicrobial sepsis in mice. Mechanistically, the scaffold protein Ahnak, which is specifically expressed in imNeu, underpins Smad7 nuclear translocation in response to IFN-γ, thus downregulating C-X-C chemokine receptor 4 expression critical for neutrophil retention in the BM. Furthermore, imNeu produce interleukin-10 to ameliorate tissue inflammation. Our findings thus reveal the ILC1-imNeu axis that protects tissues from acute inflammation due to injury or microbial infection.
    DOI:  https://doi.org/10.1038/s41467-025-61504-8
  9. Nature. 2025 Jul;643(8073): 903-905
      
    Keywords:  History; Mathematics and computing; Physics
    DOI:  https://doi.org/10.1038/d41586-025-02264-9
  10. Nat Commun. 2025 Jul 16. 16(1): 6567
      Hepatic de novo lipogenesis (DNL) is crucial for maintaining lipid homeostasis, and its dysregulation is implicated in various metabolic diseases. While it is well established that hepatic DNL is tightly regulated by hormones such as insulin and glucagon secreted from the pancreatic islets during feeding and fasting, further investigations are required to identify more hormones affecting hepatic DNL during the feeding-fasting transition. Here, we identify PRXL2A (peroxiredoxin like 2 A), an adipokine secreted during fasting, as an inhibitor of hepatic DNL. Mechanistically, PRXL2A binds to its receptor PTAFR (platelet activating factor receptor), promoting calcium mobilization and activating AMPK (AMP-activated protein kinase), thereby suppressing SREBP1 (sterol regulatory element-binding protein 1)-controlled hepatic DNL. Disruption of this axis by knockout of either Prxl2a or Ptafr increases hepatic DNL and lipid accumulation. Exogenous PRXL2A reduces hepatic DNL, suggesting a potential therapeutic strategy for diseases associated with hepatic lipid accumulation. Therefore, the PRXL2A-PTAFR signaling axis links adipose tissues and the liver to regulate hepatic lipid metabolism.
    DOI:  https://doi.org/10.1038/s41467-025-61963-z
  11. Nat Med. 2025 Jul 15.
    Global Neurodegeneration Proteomics Consortium (GNPC)
      The brain barrier system, including the choroid plexus, meninges and brain vasculature, regulates substrate transport and maintains differential protein concentrations between blood and cerebrospinal fluid (CSF). Aging and neurodegeneration disrupt brain barrier function, but proteomic studies of the effects on blood-CSF protein balance are limited. Here we used SomaScan proteomics to characterize paired CSF and plasma samples from 2,171 healthy or cognitively impaired older individuals from multiple cohorts, including the Global Neurodegeneration Proteomics Consortium. We identified proteins with correlated CSF and plasma levels that are produced primarily outside the brain and are enriched for structural domains that may enable their transport across brain barriers. CSF to plasma ratios of 848 proteins increased with aging in healthy control individuals, including complement and coagulation proteins, chemokines and proteins linked to neurodegeneration, whereas 64 protein ratios decreased with age, suggesting substrate-specific barrier regulation. Notably, elevated CSF to plasma ratios of peripherally derived or vascular-associated proteins, including DCUN1D1, MFGE8 and VEGFA, were associated with preserved cognitive function. Genome-wide association studies identified genetic loci associated with CSF to plasma ratios of 241 proteins, many of which have known disease associations, including FCN2, the collagen-like domain of which may facilitate blood-CSF transport. Overall, this work provides molecular insight into the human brain barrier system and its disruption with age and disease, with implications for the development of brain-permeable therapeutics.
    DOI:  https://doi.org/10.1038/s41591-025-03831-3
  12. Nat Immunol. 2025 Jul 16.
      Mitochondrial electron transport chain (ETC) function is linked to the generation of ATP, signaling molecules including reactive oxygen species (ROS), pyrimidines and tricarboxylic acid cycle metabolites1. Mitochondrial electron transport is required for T cell proliferation2-4. However, which mitochondrial ETC functions are necessary for each dynamic state of CD8+ T cell responses is unknown. Here we report that impairing mitochondrial complex III function, which diminishes respiration, proton pumping linked to ATP production and superoxide production, decreases peripheral naive numbers, antigen-induced CD8+ T cell proliferation and memory formation. Acute stimulation of mitochondrial complex III-deficient CD8+ T cells induced an exhausted-like phenotype. Expression of Ciona intestinalis alternative oxidase (AOX) in mitochondrial complex III-deficient CD8+ T cells restores respiration without generating ROS or proton pumping, and rescues proliferation and the exhausted phenotype but not naive or memory formation. Thus, T cell development, proliferation and memory formation have distinct requirements for mitochondrial complex III ROS.
    DOI:  https://doi.org/10.1038/s41590-025-02202-x
  13. Science. 2025 Jul 17. 389(6757): 236-237
      An antigen-presenting cell subtype tames the immune response to food antigens in early life.
    DOI:  https://doi.org/10.1126/science.adz5931
  14. Nat Commun. 2025 Jul 14. 16(1): 6496
      Innovative identification technologies for hematopoietic stem cells (HSCs) have expanded the scope of stem cell biology. Clinically, the functional quality of HSCs critically influences the safety and therapeutic efficacy of stem cell therapies. However, most analytical techniques capture only a single snapshot, disregarding the temporal context. A comprehensive understanding of the temporal heterogeneity of HSCs necessitates live-cell, real-time and non-invasive analysis. Here, we developed a prediction system for HSC diversity by integrating single-HSC ex vivo expansion technology with quantitative phase imaging (QPI)-driven machine learning. By analyzing the cellular kinetics of individual HSCs, we discovered previously undetectable diversity that snapshot analysis cannot resolve. The QPI-driven algorithm quantitatively evaluates stemness at the single-cell level and leverages temporal information to significantly improve prediction accuracy. This platform advances the field from snapshot-based identification of HSCs to dynamic, time-resolved prediction of their functional quality based on past cellular kinetics.
    DOI:  https://doi.org/10.1038/s41467-025-61846-3
  15. Science. 2025 Jul 17. eadr8628
      Diet, microbiota, and other exposures place the intestinal epithelium as a nexus for evolutionary change; however, little is known about genomic changes associated with adaptation to a uniquely human environment. Here, we interrogate the evolution of cell types in the developing human intestine by comparing tissue and organoids from humans, chimpanzees, and mice. We find that recent changes in primates are associated with immune barrier function and lipid/xenobiotic metabolism, and that human-specific genetic features impact these functions. Enhancer assays, genetic deletion, and in silico mutagenesis resolve evolutionarily significant enhancers of Lactase (LCT) and Insulin-like Growth Factor Binding Protein 2 (IGFBP2). Altogether, we identify the developing human intestinal epithelium as a rapidly evolving system, and show that great ape organoids provide insight into human biology.
    DOI:  https://doi.org/10.1126/science.adr8628
  16. Cell Metab. 2025 Jul 07. pii: S1550-4131(25)00304-3. [Epub ahead of print]
      Pancreatic alpha cells modulate beta cell function in a paracrine manner through the release of glucagon. However, the detailed molecular architecture underlying alpha-to-beta cell regulation remains poorly characterized. Here, we show that the glucagon-like peptide-1 receptor (GLP1R) is enriched as nanodomains on beta cell membranes that contact alpha cells, in keeping with increased single-molecule transcript expression. At low glucose, beta cells next to alpha cells directly sense micromolar glucagon release by pre-internalizing GLP1R. Pre-internalized GLP1R is associated with earlier beta cell Ca2+ responses to high glucose, which are then propagated across the islet. Beta cells adjacent to alpha cells are more secretory than beta cells next to other beta cells. Localized GLP1R signaling occurs in vitro and in vivo, is operative in the post-prandial state, and GLP1R contacts decrease between beta cells and alpha cells during metabolic stress. Thus, we detail a regulated pathway through which glucagon modulates insulin release.
    Keywords:  Ca(2+); GLP1R; alpha cell; beta cell; diabetes; glucagon; insulin; islet; pancreas; signaling
    DOI:  https://doi.org/10.1016/j.cmet.2025.06.009