ArticleInternational journal of medical sciences2022
Accumulation of RIPK1 into mitochondria is requisite for oxidative stress-mediated necroptosis and proliferation in Rat Schwann cells.
Article in International journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- PANoptosis in diabetes: immunometabolic insights and treatments.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondria and tumorigenesis: Molecular basis and therapeutic implications.Genes & diseases · 2026Review
- From RIPK1 to Necroptosis: Pathogenic Mechanisms in Neurodegenerative Diseases.Neurochemical research · 2025Review
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury.Neurochemical research · 2024Review
- PME-1 sensitizes glioblastoma cells to oxidative stress-induced cell death by attenuating PP2A-B55α-mediated inactivation of MAPKAPK2-RIPK1 signaling.Cell death discovery · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The injury of Schwann cells is an important pathological feature of peripheral neuropathy. However, the explicit molecular mechanism and blocking method remains to be explored. In this study, we identified an pivotal executor of necroptosis-RIPK1, performed an unique function in response to oxidative stress-induced injury in Rat Schwann cells. We found that after oxidative stress-simulation by H
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Registered trials
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