ArticleCells2019
iNOS Interacts with Autophagy Receptor p62 and is Degraded by Autophagy in Macrophages.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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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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
11 citing papers in PubMed, 25 citations in OpenAlex.
- G‑Protein-Coupled Receptor 41 (GPR41) as a Therapeutic Target for Metabolic Endotoxemia: Mechanistic Insights into AR420626-Induced Autophagy and Nuclear Factor kappa B (NF-κB) Suppression.ACS pharmacology & translational science · 2026Article
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- Ferritinophagy activation states determine the susceptibility to ferroptosis of macrophages in bone marrow and spleen.International journal of biological sciences · 2025Article
- Molecular and phenotypic distinctions of macrophages in tolerant and susceptible to hypoxia rats.PeerJ · 2023Article
- Cochlear implantation impairs intracochlear microcirculation and counteracts iNOS induction in guinea pigs.Frontiers in cellular neuroscience · 2023Article
- Inhibition of TXNDC5 attenuates lipopolysaccharide-induced septic shock by altering inflammatory responses.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Pharmacological insights into autophagy modulation in autoimmune diseases.Acta pharmaceutica Sinica. B · 2021Review
- Administration of GDF3 Into Septic Mice Improves SurvivalFrontiers in immunology · 2021Article
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- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is an important mediator of inflammation response and the production of NO has been linked to a variety of diseases, including tumors, inflammation and central nervous system diseases. In macrophages, a high level of NO is generated by iNOS during inflammatory responses triggered by cytokines or pathogens. Autophagy, a cellular bulk degradation process via lysosome, has been implicated in many disease conditions including inflammation. In this study, we have reported the previously unknown role of autophagy in regulating iNOS levels in macrophages, both under basal and Lipopolysaccharides (LPS)-induced conditions. Our data showed that iNOS levels accumulated upon autophagy inhibition and decreased upon autophagy induction. iNOS interacted and co-localized with autophagy receptor p62/SQSTM1, especially under LPS-stimulated condition in macrophages. Moreover, the immunostaining data revealed that iNOS also co-localizes with the autophagosome marker LC3 and lysosome marker LAMP1, especially under lysosomal inhibition conditions, indicating iNOS is an autophagy substrate. Finally, we showed that autophagy negatively regulated the generation of NO in macrophages, which is consistent with the changes of iNOS levels. Collectively, our study revealed a previously unknown mechanism by which autophagy regulates iNOS levels to modulate NO production during inflammation.
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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.