ArticleInflammation2018
CIDEC Is Involved in LPS-Induced Inflammation and Apoptosis in Renal Tubular Epithelial Cells.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
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- Site-specific genetic and functional signatures of aortic endothelial cells at aneurysm predilection sites in healthy and AngII ApoEAngiogenesis · 2024Article
- Intravesical BCG in patients with non-muscle invasive bladder cancer induces trained immunity and decreases respiratory infections.Journal for immunotherapy of cancer · 2023Observational
- Non-Coding RNAs in Sepsis-Associated Acute Kidney Injury.Frontiers in physiology · 2022Review
- MBD2 Mediates Septic AKI through Activation of PKCη/p38MAPK and the ERK1/2 Axis.Molecular therapy. Nucleic acids · 2021Article
- Article
- Melittin Ameliorates Endotoxin-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Cell Death in Mice.Oxidative medicine and cellular longevity · 2021Article
- The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI.Frontiers in medicine · 2021Review
- Protective Effects of Bee Venom against Endotoxemia-Related Acute Kidney Injury in Mice.Biology · 2020Article
- Protective Effects of SPA0355, a Thiourea Analogue, Against Lipopolysaccharide-Induced Acute Kidney Injury in Mice.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine 5'-monophosphate-activated protein kinase (AMPK) has been shown to have anti-inflammatory effect by inhibition of the nuclear factor κB (NF-κB) pathway and is involved in lipopolysaccharide (LPS)-induced inflammation. Cell-death-inducing DFF45-like effector C (CIDEC) can directly down-regulate AMPK activity through interacting with AMPKα subunit. However, whether the AMPK or CIDEC is involved in LPS-induced inflammation in renal tubular epithelial cells is still unknown. Therefore, we studied the role of AMPK and CIDEC in LPS-treated NRK-52E cells. Our results showed that LPS could up-regulate the expression of CIDEC in vitro and in vivo. Silencing CIDEC by CIDEC-siRNA could restore expression of phosphorylated-AMPKα which was decreased by LPS, suppress LPS-induced NF-κB pathway activation, and TNF-α, IL-6, and IL-1β production in NRK-52E cells. Furthermore, silencing CIDEC also partially alleviated LPS-induced epithelial cells apoptosis. In conclusion, the results demonstrated that CIDEC/AMPK signaling pathway played an important role in LPS-induced inflammation and epithelial cells apoptosis.
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Registered trials
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