ArticlePloS one2014
CRIF1 deficiency induces p66shc-mediated oxidative stress and endothelial activation.
Article in PloS one, 2014. 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, 19 citations in OpenAlex.
- Article
- Multifunctions of CRIF1 in cancers and mitochondrial dysfunction.Frontiers in oncology · 2022Review
- Antitumor Potential of Sericite Treatment Mediated by Cell Cycle Arrest in Triple-Negative MDA-MB231 Breast Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Mitochondria Lead the Way: Mitochondrial Dynamics and Function in Cellular Movements in Development and Disease.Frontiers in cell and developmental biology · 2021Review
- Article
- CR6-interacting factor 1 deficiency reduces endothelial nitric oxide synthase activity by inhibiting biosynthesis of tetrahydrobiopterin.Scientific reports · 2020Article
- p66shc siRNA Nanoparticles Ameliorate Chondrocytic Mitochondrial Dysfunction in Osteoarthritis.International journal of nanomedicine · 2020Article
- CRIF1 as a potential target to improve the radiosensitivity of osteosarcoma.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- CR6 interacting factor 1 deficiency promotes endothelial inflammation by SIRT1 downregulation.PloS one · 2018Article
- Differential contribution of the mitochondrial translation pathway to the survival of diffuse large B-cell lymphoma subsets.Cell death and differentiation · 2017Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction has been implicated in the pathophysiology of various cardiovascular diseases. CRIF1 is a protein present in the mitochondria associated with large mitoribosomal subunits, and CRIF1 knockdown induces mitochondrial dysfunction and promotes ROS production. p66shc is a redox enzyme implicated in mitochondrial ROS generation and translation of oxidative signals and, therefore, is a key factor for oxidative stress in endothelial cells. In this study, we investigated whether mitochondrial dysfunction induced by CRIF1 knockdown induces p66shc stimulation and plays any role in mitochondrial dysfunction-induced endothelial activation. Knockdown of CRIF1 decreased the expression of mitochondrial oxidative phosphorylation (OXPHOS) complexes I, III and IV, leading to increased mitochondrial ROS (mtROS) and hyperpolarization of the mitochondrial membrane potential. Knockdown of CRIF1 also stimulated phosphorylation of p66shc and increased cytosolic ROS in endothelial cells. Furthermore, the expression of vascular cell adhesion molecule-1 and endoplasmic reticulum stress proteins were increased upon CRIF1 knockdown in endothelial cells. However, p66shc knockdown blunted the alteration in mitochondrial dynamics and ROS production in CRIF1 knockdown endothelial cells. In addition, p66shc knockdown reduced the CRIF1 knockdown-induced increases in adhesion between monocytes and endothelial cells. Taken together, these results suggest that CRIF1 knockdown partially induces endothelial activation via increased ROS production and phosphorylation of p66shc.
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.