ArticleNature2016
Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 226 papers, 1 of them a synthesis 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
226 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- LC3-associated phagocytosis is a new strategy to inhibit picornavirus infection through increasing interferon levels and lysosomal degradation.Cellular and molecular life sciences : CMLS · 2026Article
- Identification of Novel Hub Genes Associated with Inflammation and Autophagy in Astragaloside Membranaceus ameliorates Lupus Nephritis by Bioinformatics Analysis and Molecular Dynamics Simulation.Combinatorial chemistry & high throughput screening · 2025Article
- Identification and validation of key autophagy-related genes in lupus nephritis by bioinformatics and machine learning.PloS one · 2025Article
- NADPH oxidase in B cells and macrophages protects against murine lupus by regulation of TLR7.JCI insight · 2024Article
- The Role of LC3-Associated Phagocytosis Inhibits the Inflammatory Response in Aspergillus fumigatus Keratitis.Investigative ophthalmology & visual science · 2024Article
- ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease.Autophagy · 2024Article
- Enhancement of efferocytosis through biased FPR2 signaling attenuates intestinal inflammation.EMBO molecular medicine · 2023Article
- Conditional deletion of CD25 in the corneal epithelium reveals sex differences in barrier disruption.The ocular surface · 2023Article
- LC3-associated phagocytosis promotes glial degradation of axon debris after injury in Drosophila models.Nature communications · 2023Article
- Autophagy restricts Mycobacterium tuberculosis during acute infection in mice.Nature microbiology · 2023Article
- Myeloid autophagy genes protect mice against fatal TNF- and LPS-induced cytokine storm syndromes.Autophagy · 2023Article
- Lupus Recipe inhibits cGVHD-induced lupus nephritis in mice and promote renal LC3-associated autophagy.Immunity, inflammation and disease · 2023Article
- Gene expression variability across cells and species shapes the relationship between renal resident macrophages and infiltrated macrophages.BMC bioinformatics · 2023Article
- Bioinformatic identification and validation of autophagy-related genes in rheumatoid arthritis.Clinical rheumatology · 2023Article
- Supporting the differential diagnosis of connective tissue diseases with neurological involvement by blood and cerebrospinal fluid flow cytometry.Journal of neuroinflammation · 2023Article
- AUTOPHAGY IN THE EYE: FROM PHYSIOLOGY TO PATHOPHYSOLOGY.Autophagy reports · 2023Article
- Microglia in Alzheimer's disease: pathogenesis, mechanisms, and therapeutic potentials.Frontiers in aging neuroscience · 2023Review
- Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023Review
- Regulatory mechanisms of retinal ganglion cell death in normal tension glaucoma and potential therapies.Neural regeneration research · 2023Review
166 more citing papers are in PubMed but not listed here.
Corrections and comments
- Correction · 2016-09-28Error in Image · Updated to Retraction · · see also: https://pubpeer.com/publications/29D08088B929682E80B05EB853B102
- Retraction · 2022-08-31Investigation by Company/Institution · Unreliable Data · Unreliable Image · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/29D08088B929682E80B05EB853B102
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- Erratum issued
- Retracted
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.
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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.