ArticleCell2017
Spontaneous Chitin Accumulation in Airways and Age-Related Fibrotic Lung Disease.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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
64 citing papers in PubMed, 102 citations in OpenAlex.
- Chitin Is a Potent Inducer of Type 2 Airway Inflammation Independent of Endogenous Chitinolytic Activity.Allergy · 2026Article
- Humanizing acidic mammalian chitinase variants establish lung immune conditioning and control environmentally driven inflammation and fibrosis.Cell reports · 2026Article
- Key Amino Acids Controlling pH Optima in Avian Chia Paralogs: Mechanistic Insights into Functional Divergence.Molecules (Basel, Switzerland) · 2026Article
- Generation of a Ym1 deficient mouse utilising CRISPR-Cas9 in CB6 embryos.Transgenic research · 2025Article
- The mammalian acid chitinase promotes oncogenic properties of thyroid cancer cells through the JAK2/STAT3 pathway.European thyroid journal · 2025Article
- Hyperactivation of human acidic chitinase (Chia) for potential medical use.The Journal of biological chemistry · 2025Article
- Article
- An ILC2-chitinase circuit restores lung homeostasis after epithelial injury.Science immunology · 2024Article
- Phage Immunoprecipitation-Sequencing Reveals CDHR5 Autoantibodies in Select Patients With Interstitial Lung Disease.ACR open rheumatology · 2024Article
- Fungal chitin is not an independent mediator of allergic fungal asthma severity.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Article
- Tuberculosis Severity Predictive Model Using Mtb Variants and Serum Biomarkers in a Colombian Cohort of APTB Patients.Biomedicines · 2023Article
- A type 2 immune circuit in the stomach controls mammalian adaptation to dietary chitin.Science (New York, N.Y.) · 2023Article
- Novel mechanistic insights underlying fungal allergic inflammation.PLoS pathogens · 2023Review
- Evolutionary activation of acidic chitinase in herbivores through the H128R mutation in ruminant livestock.iScience · 2023Article
- Proteins: Neglected active ingredients in edible bird's nest.Chinese herbal medicines · 2023Review
- Discovery and Optimization of a Novel Macrocyclic Amidinourea Series Active as Acidic Mammalian Chitinase Inhibitors.ACS medicinal chemistry letters · 2023Article
- The ins and outs of innate and adaptive type 2 immunity.Immunity · 2023Review
- Allergic rhinitis behavioral changes after Indonesian house dust mites allergenic extract administration as immunotherapy.Journal of public health in Africa · 2023Article
- They shall not grow mold: Soldiers of innate and adaptive immunity to fungi.Seminars in immunology · 2023Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The environmentally widespread polysaccharide chitin is degraded and recycled by ubiquitous bacterial and fungal chitinases. Although vertebrates express active chitinases from evolutionarily conserved loci, their role in mammalian physiology is unclear. We show that distinct lung epithelial cells secrete acidic mammalian chitinase (AMCase), which is required for airway chitinase activity. AMCase-deficient mice exhibit premature morbidity and mortality, concomitant with accumulation of environmentally derived chitin polymers in the airways and expression of pro-fibrotic cytokines. Over time, these mice develop spontaneous pulmonary fibrosis, which is ameliorated by restoration of lung chitinase activity by genetic or therapeutic approaches. AMCase-deficient epithelial cells express fibrosis-associated gene sets linked with cell stress pathways. Mice with lung fibrosis due to telomere dysfunction and humans with interstitial lung disease also accumulate excess chitin polymers in their airways. These data suggest that altered chitin clearance could exacerbate fibrogenic pathways in the setting of lung diseases characterized by epithelial cell dysfunction.
Indexed as
Identifiers
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.