ArticleGeroScience2022
Single-cell transcriptomics identifies premature aging features of TERC-deficient mouse brain and bone marrow.
Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- ANGPTL8 induces the aging of hematopoietic stem/progenitor cells.Biogerontology · 2026Article
- Prmt6 Deficiency Drives Osteoblast Senescence Promoting Age-Related Osteoporosis via Epigenetic Remodelling of the H3R2me2a/Sting/Ifitm3 Pathway.Journal of cellular and molecular medicine · 2026Article
- From matrix to nucleus: CD44 as a central regulator of inflammaging, autophagy, and tissue homeostasis.Biogerontology · 2026Review
- DUSP1 deficiency accelerates UVB‑induced HDF cell senescence by regulating ferroptosis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Age- and sex-dependent bone marrow adiposity and distinct transcriptional trajectories in endothelial subtypes.Scientific reports · 2026Article
- Mechanisms and disease associations of oxidative stress-mediated brain-bone axis dysregulation: a knowledge mapping and trend analysis based on Bibliometrics.Frontiers in aging neuroscience · 2026Article
- Intracerebral Hemorrhage in Aging: Pathophysiology, Clinical Challenges, and Future Directions.Life (Basel, Switzerland) · 2025Review
- Long-Term High-Fat Diet Affected Bone Marrow Microenvironment During Aging at Single-Cell Resolution.MedComm · 2025Article
- Bone marrow-derived myeloid cells drive neuroinflammation in Alzheimer's disease: Insights from the FADJournal of orthopaedic translation · 2025Article
- Single-cell profiling unveils a geroprotective role of Procyanidin C1 in hematopoietic immune system via senolytic and senomorphic effects.npj aging · 2025Article
- Senescence-induced p21Cell discovery · 2025Article
- Noncoding RNA Terc-53 and hyaluronan receptor Hmmr regulate aging in mice.Protein & cell · 2025Article
- Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression.Frontiers in oncology · 2025Review
- Single-cell transcriptomics identifies the common perturbations of monocyte/macrophage lineage cells in inflammaging of bone marrow.Journal of orthopaedic translation · 2025Article
- Single-Cell RNA-Seq Reveals the Pseudo-temporal Dynamic Evolution Characteristics of ADSCs to Neuronal Differentiation.Cellular and molecular neurobiology · 2024Article
- Insights into the Pathobiology of GM1 Gangliosidosis from Single-Nucleus Transcriptomic Analysis of CNS Cells in a Mouse Model.International journal of molecular sciences · 2024Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a progressive loss of physiological function and increased susceptibility to major pathologies. Degenerative diseases in both brain and bone including Alzheimer disease (AD) and osteoporosis are common in aging groups. TERC is RNA component of telomerase, and its deficiency accelerates aging-related phenotypes including impaired life span, organ failure, bone loss, and brain dysfunction. In this study, we investigated the traits of bone marrow-brain cross-tissue communications in young mice, natural aging mice, and premature aging (TERC deficient, TERC-KO) mice by single-cell transcriptome sequencing. Differentially expressed gene analysis of brain as well as bone marrow between premature aging mouse and young mouse demonstrated aging-related inflammatory response and suppression of neuron development. Further analysis of senescence-associated secretory phenotype (SASP) landscape indicated that TERC-KO perturbation was enriched in oligodendrocyte progenitor cells (OPCs) and hematopoietic stem and progenitor cells (HSPC). Series of inflammatory associated myeloid cells was activated in premature aging mice brain and bone marrow. Cross-tissue comparison of TERC-KO mice brain and bone marrow illustrated obvious ligand-receptor communications between brain glia cells, macrophages, and bone marrow myeloid cells in premature aging-induced inflammation. Enrichment of co-regulation modules between brain and bone marrow identified premature aging response genes such as Dusp1 and Ifitm3. Our study provides a rich resource for understanding premature aging-associated perturbation in brain and bone marrow and supporting myeloid cells and endothelial cells as promising therapy targeting for age-related brain-bone diseases.
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