ArticleNeurochemical research2018
Geniposide Increases Unfolded Protein Response-Mediating HRD1 Expression to Accelerate APP Degradation in Primary Cortical Neurons.
Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Alzheimer's Disease: From Molecular Mechanisms to Promising Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Roles of Ubiquitin Ligases and Deubiquitylases in Alzheimer's Disease.Molecular neurobiology · 2025Review
- Identification of a Selective Pharmacologic IRE1/XBP1s Activator with Enhanced Tissue Exposure.ACS chemical biology · 2025Article
- The ubiquitin-proteasome system in Alzheimer's disease: mechanism of action and current status of treatment.Frontiers in aging neuroscience · 2025Review
- Involvement of ubiquitination in Alzheimer's disease.Frontiers in neurology · 2024Review
- NeuroProtect, a Candidate Formula From Traditional Chinese Medicine, Attenuates Amyloid-Frontiers in pharmacology · 2022Article
- The emerging possibility of the use of geniposide in the treatment of cerebral diseases: a review.Chinese medicine · 2021Review
- Therapeutic Approaches Targeting Proteostasis in Kidney Disease and Fibrosis.International journal of molecular sciences · 2021Review
- Pharmacologic IRE1/XBP1s activation confers targeted ER proteostasis reprogramming.Nature chemical biology · 2020Article
- Geniposide Alleviates Isoproterenol-Induced Cardiac Fibrosis Partially via SIRT1 ActivationFrontiers in pharmacology · 2018Article
- Comparison of Rat Primary Midbrain Neurons Cultured in DMEM/F12 and Neurobasal Mediums.Basic and clinical neuroscienceArticle
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 2 institutions in 1 country.
Funding
Abstract
Altered proteostasis induced by amyloid peptide aggregation and hyperphosphorylation of tau protein, is a prominent feature of Alzheimer's disease, which highlights the occurrence of endoplasmic reticulum stress and triggers the activation of the unfolded protein response (UPR), a signaling pathway that enforces adaptive programs to sustain proteostasis. In this study, we investigated the role of geniposide in the activation of UPR induced by high glucose in primary cortical neurons. We found that high glucose induced a significant activation of UPR, and geniposide enhanced the effect of high glucose on the phosphorylation of IRE1α, the most conserved UPR signaling branch. We observed that geniposide induced the expression of HRD1, an ubiquitin-ligase E3 in a time dependent manner, and amplified the expression of HRD1 induced by high glucose in primary cortical neurons. Suppression of IRE1α activity with STF-083010, an inhibitor of IRE1 phosphorylation, prevented the roles of geniposide on the expression of HRD1 and APP degradation in high glucose-treated cortical neurons. In addition, the results from RNA interfere on HRD1 revealed that HRD1 was involved in geniposide regulating APP degradation in cortical neurons. These data suggest that geniposide might be benefit to re-establish proteostasis by enhancing the UPR to decrease the load of APP in neurons challenged by high glucose.
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.