ArticleThe Journal of pathology2020
Upregulation of Cisd2 attenuates Alzheimer's-related neuronal loss in mice.
Article in The Journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
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- Medicinal Chemistry Review of the NEET Protein Family.ChemMedChem · 2026Review
- Methylomic signatures of tau and amyloid-beta in transgenic mouse models of Alzheimer's disease neuropathology.NPJ dementia · 2026Article
- CISD2 ensures adequate ER-mitochondrial coupling, critically supporting mitochondrial function in neurons.Acta neuropathologica communications · 2025Article
- Longitudinal plasma proteomics: relation to incident Alzheimer's disease dementia and biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Article
- Upregulation of CDGSH iron sulfur domain 2 attenuates cerebral ischemia/reperfusion injury.Neural regeneration research · 2023Article
- Advances in Human Mitochondria-Based Therapies.International journal of molecular sciences · 2022Review
- Rejuvenation: Turning Back Time by Enhancing CISD2.International journal of molecular sciences · 2022Review
- CDGSH iron sulfur domain 2 mitigates apoptosis, oxidative stress and inflammatory response caused by oxygen-glucose deprivation/reoxygenation in HT22 hippocampal neurons by Akt-Nrf2-activated pathway.Metabolic brain disease · 2022Article
- Hesperetin promotes longevity and delays aging via activation of Cisd2 in naturally aged mice.Journal of biomedical science · 2022Article
- Dysregulated CaCells · 2022Review
- Long non-coding RNA NRAV enhances proliferation and invasion of hepatocellular carcinoma cells by modulating the Wnt/β-catenin signaling pathway.Bioengineered · 2022Article
- Anti-Inflammatory CDGSH Iron-Sulfur Domain 2: A Biomarker of Central Nervous System Insult in Cellular, Animal Models and Patients.Biomedicines · 2022Article
- High Expression of CISD2 in Relation to Adverse Outcome and Abnormal Immune Cell Infiltration in Glioma.Disease markers · 2022Article
- Disrupting CISD2 function in cancer cells primarily impacts mitochondrial labile iron levels and triggers TXNIP expression.Free radical biology & medicine · 2021Article
- Rejuvenating the Aging Heart by Enhancing the Expression of theInternational journal of molecular sciences · 2021Article
- Cisd2 Preserves the Youthful Pattern of the Liver Proteome during Natural Aging of Mice.Biomedicines · 2021Article
- The NFκB Antagonist CDGSH Iron-Sulfur Domain 2 Is a Promising Target for the Treatment of Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing.International journal of molecular sciences · 2020Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDGSH iron-sulfur domain-containing protein 2 (Cisd2), a protein that declines in an age-dependent manner, mediates lifespan in mammals. Cisd2 deficiency causes accelerated aging and shortened lifespan, whereas persistent expression of Cisd2 promotes longevity in mice. Alzheimer's disease (AD) is the most prevalent form of senile dementia and is without an effective therapeutic strategy. We investigated whether Cisd2 upregulation is able to ameliorate amyloid β (Aβ) toxicity and prevent neuronal loss using an AD mouse model. Our study makes three major discoveries. First, using the AD mouse model (APP/PS1 double transgenic mice), the dosage of Cisd2 appears to modulate the severity of AD phenotypes. Cisd2 overexpression (∼two-fold) significantly promoted survival and alleviated the pathological defects associated with AD. Conversely, Cisd2 deficiency accelerated AD pathogenesis. Secondly, Cisd2 overexpression protected against Aβ-mediated mitochondrial damage and attenuated loss of neurons and neuronal progenitor cells. Finally, an increase in Cisd2 shifted the expression profiles of a panel of genes that are dysregulated by AD toward the patterns observed in wild-type mice. These findings highlight Cisd2-based therapies as a potential disease-modifying strategy for AD. © 2019 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
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