ArticleNature communications2024
Mitochondrial injury induced by a Salmonella genotoxin triggers the proinflammatory senescence-associated secretory phenotype.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Sph-mediated mtDNA release and autophagy-dependent ferroptosis contribute to Staphylococcus aureus-induced mastitis.PLoS pathogens · 2026Article
- Cell senescence emerges as a hallmark and therapeutic target of chronic intracellular infection.Nature communications · 2026Article
- Review
- Honokiol-loaded nanomicelles reprogram senescence and immune evasion in hepatocellular carcinoma via SIRT3-mediated mitochondrial stabilization.Bioengineering & translational medicine · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Host mitochondrial DNA in bacterial pathogenesis: Friend, Foe, or Both?Archives of microbiology · 2026Review
- Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.NPJ biofilms and microbiomes · 2026Review
- Genomic characterization of Salmonella enterica isolates causing typhoid among Ghanaian patients.PloS one · 2026Article
- Typhoid toxin of Salmonella Typhi elicits host antimicrobial response during acute typhoid fever.EMBO molecular medicine · 2026Article
- Mitochondrial DNA released from pyroptotic synovial macrophages via DDIT3-mediated mitophagy aggravates osteoarthritis progression.Journal of orthopaedic translation · 2026Article
- KDM4A-induced tumor senescence enhances the efficacy of immunotherapy by inhibiting AGT-PHB1 axis-mediated mitophagy in colorectal cancer.Autophagy · 2025Article
- The Immunogenic Role of Self-DNA in T Cell Immunity.Clinical reviews in allergy & immunology · 2025Review
- The immune microenvironment of pathogen-associated cancers and current clinical therapeutics.Molecular cancer · 2025Review
- Reactive oxygen species and reactive nitrogen species are double-edged swords in Salmonella infection.Archives of microbiology · 2025Review
- Joint analysis of whole-genome methylation and transcriptome in avian pullorum disease and validation of gene function.BMC genomics · 2025Article
- Unraveling immunosenescence in sepsis: from cellular mechanisms to therapeutics.Cell death & disease · 2025Review
- SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis.Bone research · 2025Article
- Necrosis drives susceptibility toInfection and immunity · 2025Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Bacterial genotoxins damage host cells by targeting their chromosomal DNA. In the present study, we demonstrate that a genotoxin of Salmonella Typhi, typhoid toxin, triggers the senescence-associated secretory phenotype (SASP) by damaging mitochondrial DNA. The actions of typhoid toxin disrupt mitochondrial DNA integrity, leading to mitochondrial dysfunction and disturbance of redox homeostasis. Consequently, it facilitates the release of damaged mitochondrial DNA into the cytosol, activating type I interferon via the cGAS-STING pathway. We also reveal that the GCN2-mediated integrated stress response plays a role in the upregulation of inflammatory components depending on the STING signaling axis. These SASP factors can propagate the senescence effect on T cells, leading to senescence in these cells. These findings provide insights into how a bacterial genotoxin targets mitochondria to trigger a proinflammatory SASP, highlighting a potential therapeutic target for an anti-toxin intervention.
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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.