ArticleNature communications2025
Caspase-11 drives macrophage hyperinflammation in models of Polg-related mitochondrial disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Model organisms in POLG-related disorders: insights from yeast to multicellular systems.Cell death & disease · 2025Review
- Ubiquitous Expression ofLife (Basel, Switzerland) · 2025Article
- An inherited mitochondrial DNA mutation remodels inflammatory cytokine responses in macrophages and in vivo in mice.Nature communications · 2025Article
- Tipping the balance: innate and adaptive immunity in mitochondrial disease.Current opinion in immunology · 2025Review
- Necrosis drives susceptibility toInfection and immunity · 2025Article
- Necrosis drives susceptibility tobioRxiv : the preprint server for biology · 2024Article
- Loss-of-function mitochondrial DNA polymerase gamma variants cause vascular smooth muscle cells to secrete a diffusible mitogenic factor.Frontiers in physiology · 2024Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Mitochondrial diseases (MtD) represent a significant public health challenge due to their heterogenous clinical presentation, often severe and progressive symptoms, and lack of effective therapies. Environmental exposures, such bacterial and viral infection, can further compromise mitochondrial function and exacerbate the progression of MtD. However, the underlying immune alterations that enhance immunopathology in MtD remain unclear. Here we employ in vitro and in vivo approaches to clarify the molecular and cellular basis for innate immune hyperactivity in models of polymerase gamma (Polg)-related MtD. We reveal that type I interferon (IFN-I)-mediated upregulation of caspase-11 and guanylate-binding proteins (GBP) increase macrophage sensing of the opportunistic microbe Pseudomonas aeruginosa (PA) in Polg mutant mice. Furthermore, we show that excessive cytokine secretion and activation of pyroptotic cell death pathways contribute to lung inflammation and morbidity after infection with PA. Our work provides a mechanistic framework for understanding innate immune dysregulation in MtD and reveals potential targets for limiting infection- and inflammation-related complications in Polg-related MtD.
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