ArticleThe Journal of infectious diseases2015
Regulation of oxidative stress by methylation-controlled J protein controls macrophage responses to inflammatory insults.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Modulation of the immunogenic landscape in colorectal cancer by mitochondrial methylation-controlled J protein.Molecular biomedicine · 2026Article
- Mitochondrial Dysfunction: Unraveling the Elusive Biology Behind Anti-TNF Response During Ulcerative Colitis.Inflammatory bowel diseases · 2025Article
- Mitochondrial chaperonin DNAJC15 promotes vulnerability to ferroptosis of chemoresistant ovarian cancer cells.Open biology · 2025Article
- MCJ: A mitochondrial target for cardiac intervention in pulmonary hypertension.Science advances · 2024Article
- S-Adenosylmethionine Negatively Regulates the Mitochondrial Respiratory Chain Repressor MCJ in the Liver.International journal of biological sciences · 2024Article
- Characterizing mitochondrial features in osteoarthritis through integrative multi-omics and machine learning analysis.Frontiers in immunology · 2024Article
- An Update on the Role and Potential Molecules in Relation toDiabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Mitochondrial dysfunction-associated microbiota establishes a transmissible refractory response to anti-TNF therapy during ulcerative colitis.Gut microbes · 2023Article
- Mitochondrial complex I dysfunction alters the balance of soluble and membrane-bound TNF during chronic experimental colitis.Scientific reports · 2022Article
- Mitochondrial bioenergetics boost macrophage activation, promoting liver regeneration in metabolically compromised animals.Hepatology (Baltimore, Md.) · 2022Article
- Boosting mitochondria activity by silencing MCJ overcomes cholestasis-induced liver injury.JHEP reports : innovation in hepatology · 2021Article
- Silencing hepatic MCJ attenuates non-alcoholic fatty liver disease (NAFLD) by increasing mitochondrial fatty acid oxidation.Nature communications · 2020Article
- The mitochondrial negative regulator MCJ modulates the interplay between microbiota and the host during ulcerative colitis.Scientific reports · 2020Article
- ETV7-Mediated DNAJC15 Repression Leads to Doxorubicin Resistance in Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2018Article
- Hallmarks of Pulmonary Hypertension: Mesenchymal and Inflammatory Cell Metabolic Reprogramming.Antioxidants & redox signaling · 2018Review
- The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury.Nature communications · 2017Article
- Fine-Tuning of CD8(+) T Cell Mitochondrial Metabolism by the Respiratory Chain Repressor MCJ Dictates Protection to Influenza Virus.Immunity · 2016Article
- Deficiency of mitochondrial modulator MCJ promotes chemoresistance in breast cancer.JCI insight · 2016Article
- The effect of local anesthetic on pro-inflammatory macrophage modulation by mesenchymal stromal cells.International immunopharmacology · 2016Article
- Ikaros mediates the DNA methylation-independent silencing of MCJ/DNAJC15 gene expression in macrophages.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Mitochondria contribute to macrophage immune function through the generation of reactive oxygen species, a byproduct of the mitochondrial respiratory chain. MCJ (also known as DnaJC15) is a mitochondrial inner membrane protein identified as an endogenous inhibitor of respiratory chain complex I. Here we show that MCJ is essential for the production of tumor necrosis factor by macrophages in response to a variety of Toll-like receptor ligands and bacteria, without affecting their phagocytic activity. Loss of MCJ in macrophages results in increased mitochondrial respiration and elevated basal levels of reactive oxygen species that cause activation of the JNK/c-Jun pathway, lead to the upregulation of the TACE (also known as ADAM17) inhibitor TIMP-3, and lead to the inhibition of tumor necrosis factor shedding from the plasma membrane. Consequently, MCJ-deficient mice are resistant to the development of fulminant liver injury upon lipopolysaccharide administration. Thus, attenuation of the mitochondrial respiratory chain by MCJ in macrophages exquisitely regulates the response of macrophages to infectious insults.
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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.