ArticleJournal of cellular and molecular medicine2022
Inhibition of PKC-δ reduce rhabdomyolysis-induced acute kidney injury.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 8 citations in OpenAlex.
- PKC-δ Promotes IL-1β-Induced Apoptosis of Rat Chondrocytes and Via Activating JNK and P38 MAPK Pathways.Cartilage · 2024Article
- Inhibition of PKC-δ retards kidney fibrosis via inhibiting cGAS-STING signaling pathway in mice.Cell death discovery · 2024Article
- Inhibition of PKC-δ reduce rhabdomyolysis-induced acute kidney injury.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Despite extensive research, the mechanisms underlying rhabdomyolysis-induced acute kidney injury (AKI) remain largely elusive. In this study, we established both cell and murine models of rhabdomyolysis-induced AKI by using myoglobin and glycerin, respectively, and provided evidence that protein kinase Cδ (PKC-δ) was activated in both models and subsequently promoted cell apoptosis. Moreover, we found that this detrimental effect of PKC-δ activation can be reversed by its pharmaceutical inhibitor rottlerin. Furthermore, we detected and confirmed the existence of PKC-δ-mediated myoglobin-induced cell apoptosis and the expression of TNF-α and IL1-β via regulation of the p38MAPK and ERK1/2 signalling pathways. In summary, our research revealed the role of PKC-δ in renal cell apoptosis and suggests that PKC-δ is a viable therapeutic target for rhabdomyolysis-induced AKI.
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Registered trials
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