ArticleThe EMBO journal2018
Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency.
Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 3 of them syntheses that pooled it.
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Who cites it
126 citing papers in PubMed, 3 syntheses or guidelines pooled it, 206 citations in OpenAlex.
- Exploring the correlation between serum fibroblast growth factor-21 levels and Sarcopenia: a systematic review and meta-analysis.BMC musculoskeletal disorders · 2023Pooled it
- Liver Brain Interactions: Focus on FGF21 a Systematic Review.International journal of molecular sciences · 2022Pooled it
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- Cholesterol-driven mitochondrial rejuvenation by quercetin nanotherapeutics restores implant osseointegration in diabetes.Bioactive materials · 2026Article
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- Mitochondrial DNA release and inflammation in mitochondrial disease pathogenesis.Brain : a journal of neurology · 2026Review
- Multifunctional Role of Mitochondrial Fatty Acid Oxidation in Cancer Immunotherapy and Aging.Cancer science · 2026Review
- Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia.Journal of translational medicine · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- Improving our understanding of the biology of aging: findings from the Age-It Research Program.The journals of gerontology. Series B, Psychological sciences and social sciences · 2025Article
- Nanoparticle-mediated overexpression of RacGAP1 protects against renal ischemia/reperfusion injury by maintaining mitochondrial homeostasis.Clinical science (London, England : 1979) · 2025Article
- Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.Molecular and cellular biochemistry · 2025Article
- Sensing within: Mitochondrial inside-out signal transduction.Cell chemical biology · 2025Review
- Targeting mitochondrial structure and dynamics for therapeutic intervention in cancer.PLoS biology · 2025Article
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females.BMC cancer · 2025Article
- Altered endothelial mitochondrial Opa1-related fusion in mouse accelerates age-associated vascular and kidney damage.Physiological reports · 2025Article
- The MFN2 Q367H variant reveals a novel pathomechanism connected to mtDNA-mediated inflammation.Life science alliance · 2025Article
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.Biomolecules · 2025Review
- Mechanisms and effects of activation of innate immunity by mitochondrial nucleic acids.International immunology · 2025Review
66 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Opa1 participates in inner mitochondrial membrane fusion and cristae morphogenesis. Here, we show that muscle-specific Opa1 ablation causes reduced muscle fiber size, dysfunctional mitochondria, enhanced Fgf21, and muscle inflammation characterized by NF-κB activation, and enhanced expression of pro-inflammatory genes. Chronic sodium salicylate treatment ameliorated muscle alterations and reduced the muscle expression of Fgf21. Muscle inflammation was an early event during the progression of the disease and occurred before macrophage infiltration, indicating that it is a primary response to Opa1 deficiency. Moreover, Opa1 repression in muscle cells also resulted in NF-κB activation and inflammation in the absence of necrosis and/or apoptosis, thereby revealing that the activation is a cell-autonomous process and independent of cell death. The effects of Opa1 deficiency on the expression NF-κB target genes and inflammation were absent upon mitochondrial DNA depletion. Under Opa1 deficiency, blockage or repression of TLR9 prevented NF-κB activation and inflammation. Taken together, our results reveal that Opa1 deficiency in muscle causes initial mitochondrial alterations that lead to TLR9 activation, and inflammation, which contributes to enhanced Fgf21 expression and to growth impairment.
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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.