ReviewMedical sciences (Basel, Switzerland)2016
Neuroprotection by Endoplasmic Reticulum Stress-Induced HRD1 and Chaperones: Possible Therapeutic Targets for Alzheimer's and Parkinson's Disease.
Review in Medical sciences (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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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
15 citing papers in PubMed, 24 citations in OpenAlex.
- The Impact of REM Sleep Deprivation on ER Stress and Alzheimer-Like Pathology: Therapeutic Potential of Melatonin.Neurochemical research · 2026Article
- SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025Review
- Promotion of endoplasmic reticulum retrotranslocation by overexpression of E3 ubiquitin-protein ligase synoviolin 1 reduces endoplasmic reticulum stress and preserves cone photoreceptors in cyclic nucleotide-gated channel deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Cryptotanshinone is a candidate therapeutic agent for interstitial lung disease associated with a BRICHOS-domain mutation ofiScience · 2023Article
- Internalized Amyloid-β (1-42) Peptide Inhibits the Store-Operated Calcium Entry in HT-22 Cells.International journal of molecular sciences · 2022Article
- Keratin 8 is a scaffolding and regulatory protein of ERAD complexes.Cellular and molecular life sciences : CMLS · 2022Article
- Convergent Molecular Pathways in Type 2 Diabetes Mellitus and Parkinson's Disease: Insights into Mechanisms and Pathological Consequences.Molecular neurobiology · 2022Review
- Protein degradation-associated mechanisms that are affected in Alzheimer´s disease.Molecular and cellular biochemistry · 2022Review
- Endoplasmic Reticulum Stress and Its Role in Homeostasis and Immunity of Central and Peripheral Neurons.Frontiers in immunology · 2022Review
- Exploration of Aberrant E3 Ligases Implicated in Alzheimer's Disease and Development of Chemical Tools to Modulate Their Function.Frontiers in cellular neuroscience · 2021Review
- Pharmacological Approach for Neuroprotection After Cardiac Arrest-A Narrative Review of Current Therapies and Future Neuroprotective Cocktail.Frontiers in medicine · 2021Review
- E3 ubiquitin ligase HRD1 modulates the circadian clock through regulation of BMAL1 stability.Experimental and therapeutic medicine · 2020Article
- A Systematic Bioinformatics Workflow With Meta-Analytics Identified Potential Pathogenic Factors of Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- ATRA protects skin fibroblasts against UV‑induced oxidative damage through inhibition of E3 ligase Hrd1.Molecular medicine reports · 2019Article
- The emerging roles of protein homeostasis-governing pathways in Alzheimer's disease.Aging cell · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) and Parkinson's disease (PD) are neurodegenerative disorders with a severe medical and social impact. Further insights from clinical and scientific studies are essential to develop effective therapies. Various stresses on the endoplasmic reticulum (ER) cause unfolded/misfolded proteins to aggregate, initiating unfolded protein responses (UPR), one of which is the induction of neuronal cell death. Some of the pathogenic factors for AD and PD are associated with UPR. ER molecules such as ubiquitin ligases (E3s) and chaperones are also produced during UPR to degrade and refold aberrant proteins that accumulate in the ER. In this review, we examine the role of HMG-CoA reductase degradation protein 1 (HRD1) and the chaperone protein-disulfide isomerase (PDI), which are both produced in the ER in response to stress. We discuss the importance of HRD1 in degrading amyloid precursor protein (APP) and Parkin-associated endothelin receptor-like receptor (Pael-R) to protect against neuronal death. PDI and the chemical chaperone 4-phenyl-butyrate also exert neuroprotective effects. We discuss the pathophysiological roles of ER stress, UPR, and the induction and neuroprotective effects of HRD1 and PDI, which may represent significant targets for novel AD and PD therapies.
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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.