ArticleInternational journal of molecular sciences2021
Anakinra Activates Superoxide Dismutase 2 to Mitigate Inflammasome Activity.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Long-Term Survival of Borna Disease Virus 1 (BoDV-1)-Encephalitis: An Exceptional Case with Valuable Insights for Pathophysiology and Disease Management.Infectious diseases and therapy · 2026Article
- Deubiquitinases as Regulators and Therapeutic Targets in Vascular Diseases.International journal of molecular sciences · 2026Review
- Comparative Protective Effects of Anakinra and Tocilizumab in Experimental Ocular Ischemic Syndrome.International journal of molecular sciences · 2026Article
- Neuroprotective effects of Interleukin-1 receptor antagonism after cardiac arrest: an experimental rat study.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Interleukin-1 receptor type 1 inhibition improves blood pressure, fetal growth and immune balance in placental ischemic rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- The role of USP36 in ribosome biogenesis and other pathophysiological processes.Frontiers in molecular biosciences · 2025Review
- IL-1 receptor antagonism reveals a yin-yang relationship between NFκB and interferon signaling in chronic lymphocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- NLRP3 and cancer: Pathogenesis and therapeutic opportunities.Pharmacology & therapeutics · 2023Review
- Superoxide dismutase 2 as a predictor in patients with hepatitis B virus-associated acute-on-chronic liver failure.Clinical and experimental medicine · 2023Article
- Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Pharmacologic Management of Monogenic and Very Early Onset Inflammatory Bowel Diseases.Pharmaceutics · 2023Review
- Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs.Frontiers in immunology · 2023Review
- NLRP3 inflammasome activation in response to metals.Frontiers in immunology · 2023Review
- Mesenchymal Stromal Cells Isolated From Patients With Congenital Heart Disease Reveal an Age-Dependent Proinflammatory Phenotype.JACC. Advances · 2022Article
- Linking Genetic Diagnosis to Therapeutic Approach in Very Early Onset Inflammatory Bowel Disease: Pharmacologic Considerations.Paediatric drugs · 2022Review
- NLRP3 Inflammasome in Vascular Disease: A Recurrent Villain to Combat Pharmacologically.Antioxidants (Basel, Switzerland) · 2022Review
- Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy.The Journal of clinical investigation · 2022Article
- NLRP3 inflammasome in digestive diseases: From mechanism to therapy.Frontiers in immunology · 2022Review
- Article
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Authors and funding
16 authors at 2 institutions in 3 countries.
Funding
Abstract
Inflammasomes are powerful cytosolic sensors of environmental stressors and are critical for triggering interleukin-1 (IL-1)-mediated inflammatory responses. However, dysregulation of inflammasome activation may lead to pathological conditions, and the identification of negative regulators for therapeutic purposes is increasingly being recognized. Anakinra, the recombinant form of the IL-1 receptor antagonist, proved effective by preventing the binding of IL-1 to its receptor, IL-1R1, thus restoring autophagy and dampening NLR family pyrin domain containing 3 (NLRP3) activity. As the generation of mitochondrial reactive oxidative species (ROS) is a critical upstream event in the activation of NLRP3, we investigated whether anakinra would regulate mitochondrial ROS production. By profiling the activation of transcription factors induced in murine alveolar macrophages, we found a mitochondrial antioxidative pathway induced by anakinra involving the manganese-dependent superoxide dismutase (MnSOD) or SOD2. Molecularly, anakinra promotes the binding of SOD2 with the deubiquitinase Ubiquitin Specific Peptidase 36 (USP36) and Constitutive photomorphogenesis 9 (COP9) signalosome, thus increasing SOD2 protein longevity. Functionally, anakinra and SOD2 protects mice from pulmonary oxidative inflammation and infection. On a preclinical level, anakinra upregulates SOD2 in murine models of chronic granulomatous disease (CGD) and cystic fibrosis (CF). These data suggest that protection from mitochondrial oxidative stress may represent an additional mechanism underlying the clinical benefit of anakinra and identifies SOD2 as a potential therapeutic target.
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Registered trials
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