ArticleActa naturae
Stochastics of Degradation: The Autophagic-Lysosomal System of the Cell.
Article in Acta naturae. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Advances in Research on Autophagy in Steroid-Induced Osteonecrosis of the Femoral Head: Dual Regulation of Its Beneficial and Detrimental Effects.Drug design, development and therapy · 2026Review
- ULK1 Mediated Autophagy-Promoting Effects of Rutin-Loaded Chitosan Nanoparticles Contribute to the Activation of NF-κB Signaling Besides Inhibiting EMT in Hep3B Hepatoma Cells.International journal of nanomedicine · 2024Article
- Myelin Basic Protein Fragmentation by Engineered Human Proteasomes with Different Catalytic Phenotypes Revealed Direct Peptide Ligands of MS-Associated and Protective HLA Class I Molecules.International journal of molecular sciences · 2023Article
- Targeted protein degradation using the lysosomal pathway.RSC medicinal chemistry · 2022Review
- Intracellular Aminopeptidase Activity Determination from the Fungus Sporisorium reilianum: Purification and Biochemical Characterization of psrAPEi Enzyme.Current microbiology · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a conservative and evolutionarily ancient process that enables the transfer of various cellular compounds, organelles, and potentially dangerous cellular components to the lysosome for their degradation. This process is crucial for the recycling of energy and substrates, which are required for cellular biosynthesis. Autophagy not only plays a major role in the survival of cells under stress conditions, but is also actively involved in maintaining cellular homeostasis. It has multiple effects on the immune system and cellular remodeling during organism development. The effectiveness of autophagy is ensured by a controlled interaction between two organelles - the autophagosome and the lysosome. Despite significant progress in the description of the molecular mechanisms underlying autophagic-lysosomal system (ALS) functioning, many fundamental questions remain. Namely, the specialized functions of lysosomes and the role of ALS in the pathogenesis of human diseases are still enigmatic. Understanding of the mechanisms that are triggered at all stages of autophagic- lysosomal degradation, from the initiation of autophagy to the terminal stage of substrate destruction in the lysosome, may result in new approaches that could help better uderstand ALS and, therefore, selectively control cellular proteostasis.
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.