ReviewNature2024
A break in mitochondrial endosymbiosis as a basis for inflammatory diseases.
Review in Nature, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
85 citing papers in PubMed, 109 citations in OpenAlex.
- Living in the age of inflammation: the reverse hygiene hypothesis.Nature reviews. Immunology · 2026Article
- Cytotoxic CD4Nature aging · 2026Article
- Natural Small Molecules Targeting Mitochondrial Quality Control for the Treatment of Metabolic Diseases: Mechanisms, Novel Formulations, and Translational Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mitochondrial-Centered Biological Networks in Metabolic Disease: Toward Precision Mitochondrial Medicine.International journal of molecular sciences · 2026Review
- Spatial architecture of immunometabolism: Mitochondrial‑organelle interfaces in immune signaling (Review).International journal of molecular medicine · 2026Review
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Mitophagy mitigates mitochondrial DNA-induced activation of cGAS-STING in autoimmune thyroiditis.Nature communications · 2026Article
- Intracranial Mitochondrial Microparticles Promote Cerebral Edema via Endothelial Injury in Stroke.Translational stroke research · 2026Observational
- Mitochondrial activity promotes neutrophil degranulation and endothelial dysfunction in systemic infections.EMBO molecular medicine · 2026Article
- Review
- Mitochondrial flagella-like extensions (MitoFLARE) dysfunction triggers STING-mediated immune dysregulation in sepsis.Nature communications · 2026Article
- Mechano-metabolic feedback connects tissue fluidity to mitochondrial DNA-dependent immunity in breast cancer.Nature communications · 2026Article
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 2026Review
- Vertebral BMSC-EVs under estrogen deficiency drive senescence-related mitochondrial dysfunction in endplate chondrocytes via MRPL1 mRNA delivery.Experimental & molecular medicine · 2026Article
- Cristae: bridging bioenergetic hubs and compartmental barriers in mitochondrial homeostasis.Cell death & disease · 2026Review
- Intercellular Mitochondrial Transfer: Implications in Cardiovascular Health.Circulation research · 2026Review
- Alcohol exposure induces ferroptosis-dominated programmed cell death in esophageal epithelial cells.BMC molecular and cell biology · 2026Article
- Application of spectral flow cytometry for comprehensive detection of immune metabolism in patient-derived microsamples.Cell reports methods · 2026Article
- The human antibacterial factor APOL3 couples lysosomal damage to mitochondrial DNA efflux and type I IFN induction.Molecular cell · 2026Article
- From symbiosis to immunity: the evolutionary revival of mitochondrial defense programs in inflammatory diseases.Cell communication and signaling : CCS · 2026Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria retain bacterial traits due to their endosymbiotic origin, but host cells do not recognize them as foreign because the organelles are sequestered. However, the regulated release of mitochondrial factors into the cytosol can trigger cell death, innate immunity and inflammation. This selective breakdown in the 2-billion-year-old endosymbiotic relationship enables mitochondria to act as intracellular signalling hubs. Mitochondrial signals include proteins, nucleic acids, phospholipids, metabolites and reactive oxygen species, which have many modes of release from mitochondria, and of decoding in the cytosol and nucleus. Because these mitochondrial signals probably contribute to the homeostatic role of inflammation, dysregulation of these processes may lead to autoimmune and inflammatory diseases. A potential reason for the increased incidence of these diseases may be changes in mitochondrial function and signalling in response to such recent phenomena as obesity, dietary changes and other environmental factors. Focusing on the mixed heritage of mitochondria therefore leads to predictions for future insights, research paths and therapeutic opportunities. Thus, whereas mitochondria can be considered 'the enemy within' the cell, evolution has used this strained relationship in intriguing ways, with increasing evidence pointing to the recent failure of endosymbiosis being critical for the pathogenesis of inflammatory 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.