ReviewInternational journal of cell biology2015
Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases.
Review in International journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 82 citations in OpenAlex.
- The extracellular matrix as a dynamic regulator of brain function and plasticity.Neurobiology of disease · 2026Review
- Epigenetic Regulation of Hyaluronan-Associated Genes in the Brain: Identifying Key Regulatory Sites.Epigenomes · 2026Review
- Targeting Ischemic Stroke with Neural Stem Cells: Insights into Endogenous Repair Mechanisms, Biomaterial-Based Delivery, and Exosome Therapies.Molecular neurobiology · 2025Review
- Nicotine-Induced VEGF Levels in NSCLC Cells Are Modulated by PKA, Hyaluronan, and p53.International journal of molecular sciences · 2025Article
- Intestinal Ischemia/Reperfusion Injury Influences Hyaluronan Homeostasis in the Rat Brain.International journal of molecular sciences · 2025Article
- Article
- Development and Characterization of Hyaluronic Acid Microgels for Neural Regeneration Applications.Journal of biomedical materials research. Part A · 2025Article
- Article
- Molecular weight of hyaluronic acid crosslinked into biomaterial scaffolds affects angiogenic potential.Acta biomaterialia · 2023Article
- Endothelial Glycocalyx in Aging and Age-related Diseases.Aging and disease · 2023Review
- Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11.Cellular and molecular neurobiology · 2023Review
- A hyaluronic acid granular hydrogel nerve guidance conduit promotes regeneration and functional recovery of injured sciatic nerves in rats.Neural regeneration research · 2023Article
- Extracellular matrix and synapse formation.Bioscience reports · 2023Article
- Article
- Article
- The Role of Extracellular Matrix in Human Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Carbohydrate based biomaterials for neural interface applications.Journal of materials chemistry. B · 2022Review
- Fractone Stem Cell Niche Components Provide Intuitive Clues in the Design of New Therapeutic Procedures/Biomatrices for Neural Repair.International journal of molecular sciences · 2022Review
- Tetrodotoxin prevents heat-shock induced granule cell dispersion in hippocampal slice cultures.Frontiers in cell and developmental biology · 2022Article
- A glial perspective on the extracellular matrix and perineuronal net remodeling in the central nervous system.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The glycosaminoglycan hyaluronan (HA), a component of the extracellular matrix, has been implicated in regulating neural differentiation, survival, proliferation, migration, and cell signaling in the mammalian central nervous system (CNS). HA is found throughout the CNS as a constituent of proteoglycans, especially within perineuronal nets that have been implicated in regulating neuronal activity. HA is also found in the white matter where it is diffusely distributed around astrocytes and oligodendrocytes. Insults to the CNS lead to long-term elevation of HA within damaged tissues, which is linked at least in part to increased transcription of HA synthases. HA accumulation is often accompanied by elevated expression of at least some transmembrane HA receptors including CD44. Hyaluronidases that digest high molecular weight HA into smaller fragments are also elevated following CNS insults and can generate HA digestion products that have unique biological activities. A number of studies, for example, suggest that both the removal of high molecular weight HA and the accumulation of hyaluronidase-generated HA digestion products can impact CNS injuries through mechanisms that include the regulation of progenitor cell differentiation and proliferation. These studies, reviewed here, suggest that targeting HA synthesis, catabolism, and signaling are all potential strategies to promote CNS repair.
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.