ArticleMolecular medicine reports2017
Flow control effect of necrostatin-1 on cell death of the NRK-52E renal tubular epithelial cell line.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- An in vitro evaluation of the antioxidant activities of necroptosis and apoptosis inhibitors: the potential of necrostatin-1 and necrostatin-1i to have radical scavenging activities.Pharmacological reports : PR · 2023Article
- Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications.Pharmacological research · 2021Review
Corrections and comments
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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
Apoptosis and necroptosis occur in renal tubular epithelial cell (RTEC) death in acute kidney injury (AKI), and may be regulated by several methods. The present study identified a protective effect of necrostatin‑1 (Nec‑1) on RTECs via a flow-control-like effect. The results established a hypoxic‑ischemic injury model of rat NRK‑52E RTECs using tumour necrosis factor‑α followed by ATP depletion with antimycin A and the pan-caspase pathway blocker, benzyloxycarbonyl-Val-Ala-Asp-fluoro-methylketone. Following pre‑treatment of cells with Nec‑1, cell organelle inflation, fragmentation inhibition and improved cell viability were observed with a parallel reduced expression of microtubule‑associated protein 1A/1B‑light chain 3‑II. Nec‑1 was involved in flow control in the process of cell injury and death. In conclusion, the present study indicated that Nec‑1 provides a protective effect and serves an important role in the prevention of AKI in an NRK‑52E cell model. Further studies will be required to fully investigate the role of Nec‑1 in the development of AKI in vivo.
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Registered trials
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