ArticleCell death and differentiation2015
CR6-interacting factor 1 is a key regulator in Aβ-induced mitochondrial disruption and pathogenesis of Alzheimer's disease.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- GADD45GIP1 promotes osteosarcoma progression by modulating RPL35 ubiquitination and alleviating endoplasmic reticulum stress via the PERK/eIF2α pathway.Cancer cell international · 2025Article
- CRIF1 gene therapy ameliorates inflammatory bowel disease by suppressing TH17 cells and fibrosis through mitochondrial function regulation.Frontiers in immunology · 2025Article
- Article
- Crif1 deficiency in dopamine neurons triggers early-onset parkinsonism.Molecular psychiatry · 2023Article
- Multifunctions of CRIF1 in cancers and mitochondrial dysfunction.Frontiers in oncology · 2022Review
- Hearing Impairment in a Mouse Model of Diabetes Is Associated with Mitochondrial Dysfunction, Synaptopathy, and Activation of the Intrinsic Apoptosis Pathway.International journal of molecular sciences · 2021Article
- The role of cell type-specific mitochondrial dysfunction in the pathogenesis of Alzheimer's disease.BMB reports · 2019Review
- Red Ginseng Attenuates Aβ-Induced Mitochondrial Dysfunction and Aβ-mediated Pathology in an Animal Model of Alzheimer's Disease.International journal of molecular sciences · 2019Article
- Article
- Thrombospondin-1 protects against Aβ-induced mitochondrial fragmentation and dysfunction in hippocampal cells.Cell death discovery · 2018Article
- p73 Regulates Primary Cortical Neuron Metabolism: a Global Metabolic Profile.Molecular neurobiology · 2018Article
- Targeted deletion of Crif1 in mouse epidermis impairs skin homeostasis and hair morphogenesis.Scientific reports · 2017Article
- Annexin A1 restores AβAging cell · 2017Article
- Article
- Co-Activation of PKC-δ by CRIF1 Modulates Oxidative Stress in Bone Marrow Multipotent Mesenchymal Stromal Cells after Irradiation by Phosphorylating NRF2 Ser40.Theranostics · 2017Article
- Lipid microdomain modification sustains neuronal viability in models of Alzheimer's disease.Acta neuropathologica communications · 2016Article
- Alzheimer's Disease: From Mitochondrial Perturbations to Mitochondrial Medicine.Brain pathology (Zurich, Switzerland) · 2016Review
- Insulin-degrading enzyme secretion from astrocytes is mediated by an autophagy-based unconventional secretory pathway in Alzheimer disease.Autophagy · 2016Article
- Mitochondrial Dynamics and Heart Failure.Comprehensive Physiology · 2015Review
- Statins induce insulin-degrading enzyme secretion from astrocytes via an autophagy-based unconventional secretory pathway.Molecular neurodegeneration · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction, often characterized by massive fission and other morphological abnormalities, is a well-known risk factor for Alzheimer's disease (AD). One causative mechanism underlying AD-associated mitochondrial dysfunction is thought to be amyloid-β (Aβ), yet the pathways between Aβ and mitochondrial dysfunction remain elusive. In this study, we report that CR6-interacting factor 1 (Crif1), a mitochondrial inner membrane protein, is a key player in Aβ-induced mitochondrial dysfunction. Specifically, we found that Crif1 levels were downregulated in the pathological regions of Tg6799 mice brains, wherein overexpressed Aβ undergoes self-aggregation. Downregulation of Crif1 was similarly observed in human AD brains as well as in SH-SY5Y cells treated with Aβ. In addition, knockdown of Crif1, using RNA interference, induced mitochondrial dysfunction with phenotypes similar to those observed in Aβ-treated cells. Conversely, Crif1 overexpression prevented Aβ-induced mitochondrial dysfunction and cell death. Finally, we show that Aβ-induced downregulation of Crif1 is mediated by enhanced reactive oxygen species (ROS) and ROS-dependent sumoylation of the transcription factor specificity protein 1 (Sp1). These results identify the ROS-Sp1-Crif1 pathway to be a new mechanism underlying Aβ-induced mitochondrial dysfunction and suggest that ROS-mediated downregulation of Crif1 is a crucial event in AD pathology. We propose that Crif1 may serve as a novel therapeutic target in the treatment of AD.
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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.