ArticleInternational urology and nephrology2018
Down-regulation of GRP78 alleviates lipopolysaccharide-induced acute kidney injury.
Article in International urology and nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Toward Combinatorial Strategies to Improve Proximal Tubule Recovery Following Acute Kidney Injury.Seminars in nephrology · 2026Review
- Ebselen Alleviates Sepsis-Induced Acute Kidney Injury by Regulating Endoplasmic Reticulum Stress, Apoptosis, and Oxidative Stress.Veterinary medicine and science · 2025Article
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- Role and mechanism of endoplasmic reticulum stress and NLRP3 inflammasome in acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Forsythiaside A ameliorates sepsis-induced acute kidney injury via anti-inflammation and antiapoptotic effects by regulating endoplasmic reticulum stress.BMC complementary medicine and therapies · 2023Article
- Remifentanil attenuates endoplasmic reticulum stress and inflammatory injury in LPS-induced damage in HK-2 cells.Renal failure · 2022Article
- Siah2-GRP78 interaction regulates ROS and provides a proliferative advantage to Helicobacter pylori-infected gastric epithelial cancer cells.Cellular and molecular life sciences : CMLS · 2022Article
- The diagnostic value of endoplasmic reticulum stress-related specific proteins GRP78 and CHOP in patients with sepsis: a diagnostic cohort study.Annals of translational medicine · 2022Article
- Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice.Experimental and therapeutic medicine · 2022Article
- Effects of folic acid on oxidative damage of kidney in lead-exposed rats.Frontiers in nutrition · 2022Article
- Endoplasmic reticulum stress regulates cell injury in lipopolysaccharide-induced nerve cells.The Journal of international medical research · 2020Article
- Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function.EBioMedicine · 2018Article
- Methane-Rich Saline Ameliorates Sepsis-Induced Acute Kidney Injury through Anti-Inflammation, Antioxidative, and Antiapoptosis Effects by Regulating Endoplasmic Reticulum Stress.Oxidative medicine and cellular longevity · 2018Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAcute kidney injury (AKI) is accompanied with life-threatening sepsis. It is necessary to develop effective therapy agent or strategy for treating AKI. LPS is a primary pathogenic factor that induces sepsis. Glucose-regulated protein 78 (GRP78) is closely related to cell injuries. The objective of this study was to examine the role of GRP78 in LPS-induced AKI.
methodsCell counting kit-8 (CCK-8) assay and flow cytometry (FCM) were respectively performed to assess the cell viability and apoptosis. Available commercial kits were used to detect the reactive oxygen species (ROS) contents and the activity of oxidative indicators. The expressions of the relevant factors were determined by real-time PCR (RT-PCR) and Western blot.
resultsThe results showed that the expression of GRP78 was apparently increased by LPS treatment, and that the down-regulation of GRP78 by small RNA interference improved the proliferation ability of renal cells in comparison to LPS group. The LPS-induced immune response and oxidative stress was alleviated by the depletion of GRP78. Moreover, the LPS-induced apoptosis was reduced in the GRP78 group by regulating the expression of mitochondrial apoptosis (Bcl-2, Bax) and endoplasmic reticulum (ER) stress (CHOP, caspase-12)-associated proteins. In addition, the protective role of GRP78 reduction was partly related to the balance of NF-κB/IκB.
conclusionsDown-regulation of GRP78 attenuated LPS-induced AKI through inhibiting immune response/oxidative stress-associated apoptosis.
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.