ReviewACS chemical neuroscience2019
SQSTM1/p62: A Potential Target for Neurodegenerative Disease.
Review in ACS chemical neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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.
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Who cites it
99 citing papers in PubMed, 188 citations in OpenAlex.
- Therapeutic potential and underlying mechanisms of engineered young plasma-derived exosomes in Alzheimer's disease.Bioactive materials · 2027Article
- Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Mushrooms as potent autophagy modulators in cancer therapy: Current evidence and therapeutic prospects.Cancer pathogenesis and therapy · 2026Review
- Unraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach.Histology and histopathology · 2026Article
- Cullin-3 adaptor SHKBP1 inhibits SQSTM1/p62 oligomerization and Keap1 sequestration.The Journal of cell biology · 2026Article
- Crosstalk Between the NRF2 Signaling Pathway and Heat Shock Proteins: Implications for Cellular Stress Response and Disease Therapy.Oxidative medicine and cellular longevity · 2026Review
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- Peripheral and CSF protein quantification in Parkinson's disease and multiple system atrophy-the nucleic acid-linked immuno-sandwich assay.Brain communications · 2026Article
- Missense variant in TTBK2 kinase domain causes loss of function and impaired protein phosphorylation.Scientific reports · 2025Article
- Implementing N-terminomics and machine learning to probe Nt-arginylation.Nature communications · 2025Article
- The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases.Progress in neurobiology · 2025Review
- Article
- Caspase-independent cell death in lung cancer: from mechanisms to clinical applications.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Investigation of the Effects of Acacetin on Autophagy Pathway and Exosome Release in Amyloid Beta Peptide-Induced Toxicity Models.Molecular neurobiology · 2025Article
- The Role of Autophagy in Long-term Effects of Spinal Cord Injury: Does Exosome Change the Autophagy Process and Vice Versa?Advanced pharmaceutical bulletin · 2025Review
- p62 Binding to Protein Kinase C Regulates HIV-1 gp120 V3 Loop Induced Microglial Inflammation.Inflammation · 2025Article
- MiR-124 Delivered by Extracellular Vesicles from Mesenchymal Stem Cell Exerts Neuroprotective Effects by Stabilizing the p62-Keap1-Nrf2 Pathway after Spinal Cord Injury in Rats.Molecular neurobiology · 2025Article
- Intramyocardial injection of pre-cultured endothelial progenitor cells and mesenchymal stem cells inside alginate/gelatin microspheres induced angiogenesis in infarcted rabbits.Cell communication and signaling : CCS · 2025Article
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Aberrant aging-associated p62 autophagic cascade in biopsied olfactory neuronal cells from patients with psychosis.Schizophrenia (Heidelberg, Germany) · 2025Article
39 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegenerative diseases, characterized by a progressive loss of brain function, affect the lives of millions of individuals worldwide. The complexity of the brain poses a challenge for scientists trying to map the biochemical and physiological pathways to identify areas of pathological errors. Brain samples of patients with neurodegenerative diseases have been shown to contain large amounts of misfolded and abnormally aggregated proteins, resulting in dysfunction in certain brain centers. Removal of these abnormal molecules is essential in maintaining protein homeostasis and overall neuronal health. Macroautophagy is a major route by which cells achieve this. Administration of certain autophagy-enhancing compounds has been shown to provide therapeutic effects for individuals with neurodegenerative conditions. SQSTM1/p62 is a scaffold protein closely involved in the macroautophagy process. p62 functions to anchor the ubiquitinated proteins to the autophagosome membrane, promoting degradation of unwanted molecules. Modulators targeting p62 to induce autophagy and promote its protective pathways for aggregate protein clearance have high potential in the treatment of these conditions. Additionally, causal relationships have been found between errors in regulation of SQSTM1/p62 and the development of a variety of neurodegenerative disorders, including Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, and frontotemporal lobar degeneration. Furthermore, SQSTM1/p62 also serves as a signaling hub for multiple pathways associated with neurodegeneration, providing a potential therapeutic target in the treatment of neurodegenerative diseases. However, rational design of a p62-oriented autophagy modulator that can balance the negative and positive functions of multiple domains in p62 requires further efforts in the exploration of the protein structure and pathological basis.
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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.