ReviewSeminars in immunopathology2015
Protein misfolding and dysregulated protein homeostasis in autoinflammatory diseases and beyond.
Review in Seminars in immunopathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Unveiling the dark side of glucose-regulated protein 78 (GRP78) in cancers and other human pathology: a systematic review.Molecular medicine (Cambridge, Mass.) · 2023Pooled it
- Autophagy targeted nano-medicine in norphytane atrophic arthritis model: Beclin1/XBP/PTEN/STAT-3A genetic profile.Future science OA · 2026Article
- Targeting the Gut-Liver Mitochondria Axis in MASLD: Mechanisms and Therapeutic Perspectives.Current medical science · 2026Review
- Oxidized low-density lipoprotein causes ribosome reduction and inhibition of protein synthesis in retinal pigment epithelial cells.Biochemistry and biophysics reports · 2022Article
- Management of Atrial Fibrillation Using Immunoglobulin Free Light Chains, Novel Biomarkers of Inflammation.European cardiology · 2022Review
- CRYPTOCHROMES promote daily protein homeostasis.The EMBO journal · 2022Article
- Dexmedetomidine Mitigated NLRP3-Mediated NeuroinflammationFrontiers in pharmacology · 2021Article
- Inflammasomes and Proteostasis Novel Molecular Mechanisms Associated With Atrial Fibrillation.Circulation research · 2020Review
- Moving towards a systems-based classification of innate immune-mediated diseases.Nature reviews. Rheumatology · 2020Review
- Genes expression profiling of alveolar macrophages exposed to non-functionalized, anionic and cationic multi-walled carbon nanotubes shows three different mechanisms of toxicity.Journal of nanobiotechnology · 2020Article
- KLICK Syndrome Linked to aFrontiers in immunology · 2020Review
- Baldspot/ELOVL6 is a conserved modifier of disease and the ER stress response.PLoS genetics · 2018Article
- Inhibitor of apoptosis proteins are required for effective fusion of autophagosomes with lysosomes.Cell death & disease · 2018Article
- Inositol-Requiring Enzyme 1-Mediated Downregulation of MicroRNA (miR)-146a and miR-155 in Primary Dermal Fibroblasts across ThreeFrontiers in immunology · 2018Article
- Design of coiled-coil protein-origami cages that self-assemble in vitro and in vivo.Nature biotechnology · 2017Article
- Interplay of endoplasmic reticulum stress and autophagy in neurodegenerative disorders.Autophagy · 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cells have a number of mechanisms to maintain protein homeostasis, including proteasome-mediated degradation of ubiquitinated proteins and autophagy, a regulated process of "self-eating" where the contents of entire organelles can be recycled for other uses. The unfolded protein response prevents protein overload in the secretory pathway. In the past decade, it has become clear that these fundamental cellular processes also help contain inflammation though degrading pro-inflammatory protein complexes such as the NLRP3 inflammasome. Signaling pathways such as the UPR can also be co-opted by toll-like receptor and mitochondrial reactive oxygen species signaling to induce inflammatory responses. Mutations that alter key inflammatory proteins, such as NLRP3 or TNFR1, can overcome normal protein homeostasis mechanisms, resulting in autoinflammatory diseases. Conversely, Mendelian defects in the proteasome cause protein accumulation, which can trigger interferon-dependent autoinflammatory disease. In non-Mendelian inflammatory diseases, polymorphisms in genes affecting the UPR or autophagy pathways can contribute to disease, and in diseases not formerly considered inflammatory such as neurodegenerative conditions and type 2 diabetes, there is increasing evidence that cell intrinsic or environmental alterations in protein homeostasis may contribute to pathogenesis.
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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.