ArticleThe Journal of biological chemistry2013
Endothelin-converting enzymes degrade intracellular β-amyloid produced within the endosomal/lysosomal pathway and autophagosomes.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 85 citations in OpenAlex.
- Article
- Endothelin-converting enzyme 2 regulates κ opioid receptor trafficking and function.The Journal of pharmacology and experimental therapeutics · 2025Article
- Review
- Potential Mechanisms of Tunneling Nanotube Formation and Their Role in Pathology Spread in Alzheimer's Disease and Other Proteinopathies.International journal of molecular sciences · 2024Review
- Nascent Aβ42 Fibrillization in Synaptic Endosomes Precedes Plaque Formation in a Mouse Model of Alzheimer's-like β-Amyloidosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Pathogenesis of Chronic Kidney Disease Is Closely Bound up with Alzheimer's Disease, Especially via the Renin-Angiotensin System.Journal of clinical medicine · 2023Review
- Neuroprotective Effects and Therapeutic Potential of the Citrus Flavonoid Hesperetin in Neurodegenerative Diseases.Nutrients · 2022Review
- Neuroprotective Effect of Carnosine Is Mediated by Insulin-Degrading Enzyme.ACS chemical neuroscience · 2022Article
- Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine.The EPMA journal · 2021Review
- Endosomal-lysosomal dysfunctions in Alzheimer's disease: Pathogenesis and therapeutic interventions.Metabolic brain disease · 2021Review
- Linking Oxidative Stress and Proteinopathy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Endothelin ETInternational journal of molecular sciences · 2021Review
- Therapeutic Effect of Endothelin-Converting Enzyme Inhibitor on Chronic Kidney Disease through the Inhibition of Endoplasmic Reticulum Stress and the NLRP3 Inflammasome.Biomedicines · 2021Article
- The emerging roles of vacuolar-type ATPase-dependent Lysosomal acidification in neurodegenerative diseases.Translational neurodegeneration · 2020Review
- ECE2 regulates neurogenesis and neuronal migration during human cortical development.EMBO reports · 2020Article
- Oligomerization and Conformational Change Turn Monomeric β-Amyloid and Tau Proteins Toxic: Their Role in Alzheimer's Pathogenesis.Molecules (Basel, Switzerland) · 2020Review
- Identification of Alzheimer's disease-associated rare coding variants in the ECE2 gene.JCI insight · 2020Article
- Evaluation of Toxic Amyloid 42 Oligomers in Rat Primary Cerebral Cortex Cells and Human iPS-derived Neurons Treated with 10-Me-Aplog-1, a New PKC Activator.International journal of molecular sciences · 2020Article
- A Systematic Bioinformatics Workflow With Meta-Analytics Identified Potential Pathogenic Factors of Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- Targeting amyloid clearance in Alzheimer's disease as a therapeutic strategy.British journal of pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Impairments in Aβ removal are increasingly being considered as a possible cause for the abnormal Aβ build-up typical of Alzheimer disease. Of particular interest is a pool of Aβ that accumulates intraneuronally and may contribute to neuronal toxicity. The mechanism for intraneuronal accumulation, however, is not well understood and is commonly attributed to impaired removal of extracellular Aβ by neurons. Based on the intracellular distribution of the well established Aβ degrading enzymes, ECE-1 and ECE-2, we tested whether impairments in their catalytic activity could lead to intracellular Aβ accumulation. Using SH-SY5Y cells overexpressing wild-type amyloid precursor protein and pharmacological inhibition of endogenous ECE activity, we found that ECEs participate in the degradation of at least two distinct pools of Aβ; one destined for secretion and the other being produced and degraded within the endosomal-autophagic-lysosomal pathways. Although ECE-1 regulates both pools of Aβ, ECE-2 regulates mainly the intracellular pool of the peptide. Consistent with this result, ECE-2 was found to co-localize with markers of the endosomal/lysosomal pathway but not with a trans-Golgi network marker. Furthermore, ECE-2 was detected in autophagic vesicles in cells treated with chloroquine. Under these conditions, ECE inhibition produced significantly higher elevations in intracellular Aβ than chloroquine treatment alone. This study highlights the existence of Aβ clearance mechanisms by ECEs at intracellular sites of production. Alterations in ECE activity may be considered as a cause for increased intraneuronal Aβ in Alzheimer disease.
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.