ReviewSeminars in immunology2012
New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.
Review in Seminars in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.
- Mitochondrial Dysfunction and Cognitive Impairment in Schizophrenia: The Role of Inflammation.Schizophrenia bulletin · 2025Pooled it
- Pooled it
- Oxidative Stress and Cancer Risk in Schistosomiasis.Oxidative medicine and cellular longevity · 2024Review
- Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy.Journal of hematology & oncology · 2023Review
- Effective Modulation of Inflammation and Oxidative Stress for Enhanced Regeneration of Intervertebral Discs Using 3D Porous Hybrid Protein Nanoscaffold.Advanced materials (Deerfield Beach, Fla.) · 2023Article
- Anti-inflammatory and anti-COVID-19 effect of a novel polyherbal formulation (Imusil) via modulating oxidative stress, inflammatory mediators and cytokine storm.Inflammopharmacology · 2022Article
- Review
- Molecular and Supramolecular Structure of the Mitochondrial Oxidative Phosphorylation System: Implications for Pathology.Life (Basel, Switzerland) · 2021Review
- Genetic Defects and Pro-inflammatory Cytokines in Parkinson's Disease.Frontiers in neurology · 2021Review
- Revisiting TNF Receptor-Associated Periodic Syndrome (TRAPS): Current Perspectives.International journal of molecular sciences · 2020Review
- Reactive Oxygen Species Are Key Mediators of Demyelination in Canine Distemper Leukoencephalitis but not in Theiler's Murine Encephalomyelitis.International journal of molecular sciences · 2019Article
- Peroxiredoxins in Cancer and Response to Radiation Therapies.Antioxidants (Basel, Switzerland) · 2019Review
- Mitochondria as a therapeutic target for common pathologies.Nature reviews. Drug discovery · 2018Review
- Adolescent Binge Alcohol Exposure Affects the Brain Function Through Mitochondrial Impairment.Molecular neurobiology · 2018Article
- DeSUMOylation of MKK7 kinase by the SUMO2/3 protease SENP3 potentiates lipopolysaccharide-induced inflammatory signaling in macrophages.The Journal of biological chemistry · 2018Article
- Pinocembrin Suppresses HMolecular neurobiology · 2018Article
- TLR4-NOX2 axis regulates the phagocytosis and killing of Mycobacterium tuberculosis by macrophages.BMC pulmonary medicine · 2017Article
- Methionine and methionine sulfoxide treatment induces M1/classical macrophage polarization and modulates oxidative stress and purinergic signaling parameters.Molecular and cellular biochemistry · 2017Article
- Streptococcus sanguinis induces neutrophil cell death by production of hydrogen peroxide.PloS one · 2017Article
- Immunometabolism and autoimmunity.Immunology and cell biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) such as superoxide (O(2)(-)) and hydrogen peroxide (H(2)O(2)) have long been implicated as pro-inflammatory, yet the sources of ROS and the molecular mechanisms by which they enhance inflammation have been less clear. Recent advances in the understanding of the molecular basis of inflammation mediated by the innate immune system have allowed these issues to be revisited. Although the Nox2 NADPH oxidases generate the bulk of ROS for antimicrobial host defense, recent studies have found that NADPH oxidase-dependent ROS production can actually dampen macrophage inflammatory responses to sterile pro-inflammatory stimuli. Instead, production of mitochondrial ROS has emerged as an important factor in both host defense and sterile inflammation. Excess mitochondrial ROS can be generated by either damage to the respiratory chain or by alterations of mitochondrial function such as those that increase membrane potential and reduce respiratory electron carriers. In autoinflammatory diseases, where key components of innate immune responses are activated by genetic mutations or environmental stimuli, inflammation has been found to be particularly sensitive to inhibition of mitochondrial ROS production. These findings have highlighted mitochondrial ROS as a novel generator of pro-inflammatory ROS and a potential therapeutic target in inflammatory diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.