For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
2
views
32
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      324
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Transcutaneous Electrical Acupoint Stimulation Ameliorates Cognitive Function through PINK1/Parkin Mediated Mitophagy in VD Rats

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In this study, we investigated whether transcutaneous electrical acupoint stimulation (TEAS) could improve cognitive function in VD rats by regulating PINK1/Parkin-mediated mitophagy. VD rat model was prepared by modified 2-vessel occlusion (2-VO) and randomly divided into four groups: Sham group (Sham), Model group (Model), TEAS group (TEAS), and TEAS + 3-MA group (T +3 -MA). In the T +3 -MA group, autophagy inhibitor (3-MA) was injected into the lateral ventricle. After modeling, Y maze (YM), new object recognition test (NORT), Morris water maze (MWM), immunofluorescence, and Western blot were used to observe the effects of TEAS on VD rats. Behavioral experiments revealed that TEAS effectively improved the learning and memory ability of VD rats. Immunofluorescence results showed that TEAS could upregulate LC3 expression. Western blot results showed that TEAS upregulated the expression of PINK1, Parkin, and LC3-II, and downregulated the expression of LC3-I and p62 in VD rats. T +3 -MA group shows the opposite trend to TEAS group. This study demonstrates that TEAS ameliorates cognitive function through PINK1/Parkin-mediated mitophagy in VD rats.

          Related collections

          Most cited references32

          • Record: found
          • Abstract: found
          • Article: not found

          Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease

          Evandro F Fang, Yujun Hou, Konstantinos Palikaras … (2019)
          Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). The molecular mechanisms of impaired mitochondrial homeostasis in AD are being investigated. Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models. In both amyloid-β (Aβ) and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD+ supplementation, urolithin A, and actinonin) reverses memory impairment through PINK-1 (PTEN-induced kinase-1)-, PDR-1 (Parkinson's disease-related-1; parkin)-, or DCT-1 (DAF-16/FOXO-controlled germline-tumor affecting-1)-dependent pathways. Mitophagy diminishes insoluble Aβ1-42 and Aβ1-40 and prevents cognitive impairment in an APP/PS1 mouse model through microglial phagocytosis of extracellular Aβ plaques and suppression of neuroinflammation. Mitophagy enhancement abolishes AD-related tau hyperphosphorylation in human neuronal cells and reverses memory impairment in transgenic tau nematodes and mice. Our findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and that mitophagy represents a potential therapeutic intervention.
          Article 0 comments Cited 499 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            PINK1/Parkin-mediated mitophagy in mammalian cells.

            Akinori Eiyama, Koji Okamoto (2015)
            Mitochondria-specific autophagy (mitophagy) is a fundamental process critical for maintaining mitochondrial fitness in a myriad of cell types. Particularly, mitophagy contributes to mitochondrial quality control by selectively eliminating dysfunctional mitochondria. In mammalian cells, the Ser/Thr kinase PINK1 and the E3 ubiquitin ligase Parkin act cooperatively in sensing mitochondrial functional state and marking damaged mitochondria for disposal via the autophagy pathway. Notably, ubiquitin and deubiquitinases play vital roles in modulating Parkin activity and mitophagy efficiency. In this review, we highlight recent breakthroughs addressing the key issues of how PINK1 activates Parkin in response to mitochondrial malfunction, how Parkin localizes specifically to impaired mitochondria, and how ubiquitination and deubiquitination regulate PINK1/Parkin-mediated mitophagy.
            Article 0 comments Cited 221 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              PINK1/PARKIN signalling in neurodegeneration and neuroinflammation

              Peter M. J. Quinn, Paula Moreira, António Ambrósio … (2020)
              Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson’s disease (PD). PINK1, a protein kinase, and PARKIN, an E3 ubiquitin ligase, control the specific elimination of dysfunctional or superfluous mitochondria, thus fine-tuning mitochondrial network and preserving energy metabolism. PINK1 regulates PARKIN translocation in impaired mitochondria and drives their removal via selective autophagy, a process known as mitophagy. As knowledge obtained using different PINK1 and PARKIN transgenic animal models is being gathered, growing evidence supports the contribution of mitophagy impairment to several human pathologies, including PD and Alzheimer’s diseases (AD). Therefore, therapeutic interventions aiming to modulate PINK1/PARKIN signalling might have the potential to treat these diseases. In this review, we will start by discussing how the interplay of PINK1 and PARKIN signalling helps mediate mitochondrial physiology. We will continue by debating the role of mitochondrial dysfunction in disorders such as amyotrophic lateral sclerosis, Alzheimer’s, Huntington’s and Parkinson’s diseases, as well as eye diseases such as age-related macular degeneration and glaucoma, and the causative factors leading to PINK1/PARKIN-mediated neurodegeneration and neuroinflammation. Finally, we will discuss PINK1/PARKIN gene augmentation possibilities with a particular focus on AD, PD and glaucoma.
              Article 0 comments Cited 92 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Youliang Wen:
                ORCID: https://orcid.org/0000-0002-5425-5063
                Journal
                Journal ID (nlm-ta): Evid Based Complement Alternat Med
                Journal ID (iso-abbrev): Evid Based Complement Alternat Med
                Journal ID (publisher-id): ECAM
                Title: Evidence-based Complementary and Alternative Medicine : eCAM
                Publisher: Hindawi
                ISSN (Print): 1741-427X
                ISSN (Electronic): 1741-4288
                Publication date Collection: 2022
                Publication date (Electronic): 3 June 2022
                Publication date PMC-release: 3 June 2022
                Volume: 2022
                Electronic Location Identifier: 2810794
                Affiliations
                1School of Rehabilitation Medicine, Gannan Medical University, Ganzhou, Jiangxi 341000, China
                2Research Center of Integrated Traditional Chinese and Western Medicine, Gannan Medical University, Ganzhou, Jiangxi 341000, China
                3Department of Rehabilitation Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, China
                4College of Physical Education and Health Sciences, Zhejiang Normal University, Jinhua, Zhejiang 321004, China
                5Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, Ganzhou, Jiangxi 341000, China
                6Ganzhou Key Laboratory of Rehabilitation Medicine, Gannan Medical University, Ganzhou, Jiangxi 341000, China
                Author notes

                Academic Editor: Weidong Pan

                Author information
                https://orcid.org/0000-0002-5425-5063
                Article
                DOI: 10.1155/2022/2810794
                PMC ID: 9187477
                PubMed ID: 35692579
                SO-VID: 95260458-0313-42b2-9aae-5f122aabdfc6
                Copyright © Copyright © 2022 Ziwei Hu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 December 2021
                Date accepted : 11 May 2022
                Funding
                Funded by: Gannan Medical University
                Award ID: QD201501
                Funded by: Natural Science Foundation of Jiangxi Provincial Science
                Award ID: 20192BAB205082
                Funded by: Chinese and Western Medicine Applied Rehabilitation Therapy Team
                Award ID: TS202005
                Funded by: Treasure of Traditional Chinese Medicine-Moxibustion Development Booster
                Award ID: 202110413003
                Funded by: FM combined with SET in the treatment of postpartum low back pain
                Award ID: YC2021-X017
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Complementary & Alternative medicine
                Data availability:
                ScienceOpen disciplines: Complementary & Alternative medicine

                Comments

                Comment on this article

                scite_

                Similar content324

                See all similar

                Cited by1

                See all cited by

                Most referenced authors391

                See all reference authors