ArticleNature aging2024
Aging-induced MCPH1 translocation activates necroptosis and impairs hematopoietic stem cell function.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 6 citations in OpenAlex.
- Aging mechanisms and rejuvenation strategies for hematopoietic stem cells.Genome biology · 2026Review
- Mutation of Tubgcp6 induces hematopoietic stem and progenitor cell exhaustion in zebrafish.Communications biology · 2026Article
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Non-necroptotic MLKL function damages mitochondria and promotes hematopoietic stem cell aging.Nature communications · 2026Article
- Aging-declined RNA exportation impairs hematopoietic stem cells by inducing R-loop.Haematologica · 2026Article
- Hematopoietic Stem Cell Aging: Mechanisms, Microenvironment Influences, and Rejuvenation Strategies.Bioengineering (Basel, Switzerland) · 2025Review
- A Study of Skeletal Stem Cell Dynamics and Its Potential Applications in the Design of a Titanium Implant for Senile Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling immunosenescence in sepsis: from cellular mechanisms to therapeutics.Cell death & disease · 2025Review
- Adhesive and injectable hydrogel microspheres for NRF2-mediated periodontal bone regeneration.International journal of oral science · 2025Article
- An NADNature aging · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
DNA damage contributes to the aging of hematopoietic stem cells (HSCs), yet the underlying molecular mechanisms are not fully understood. In this study, we identified a heterogeneous functional role of microcephalin (MCPH1) in the nucleus and cytoplasm of mouse HSCs. In the nucleus, MCPH1 maintains genomic stability, whereas in the cytoplasm, it prevents necroptosis by binding with p-RIPK3. Aging triggers MCPH1 translocation from cytosol to nucleus, reducing its cytoplasmic retention and leading to the activation of necroptosis and deterioration of HSC function. Mechanistically, we found that KAT7-mediated lysine acetylation within the NLS motif of MCPH1 in response to DNA damage facilitates its nuclear translocation. Targeted mutation of these lysines inhibits MCPH1 translocation and, consequently, compromises necroptosis. The dysfunction of necroptosis signaling, in turn, improves the function of aged HSCs. In summary, our findings demonstrate that DNA damage-induced redistribution of MCPH1 promotes HSC aging and could have broader implications for aging and aging-related diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.