ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023
Genetic and pharmacological inhibition of GRPR protects against acute kidney injury via attenuating renal inflammation and necroptosis.
Open access · greenAbstract read
In one paragraph
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Loss of KLF15 expression characterizes proximal tubule injury in cisplatin-induced acute kidney injury: A multi-omics study.Current research in toxicology · 2026Article
- The JAK1-STAT1 signaling pathway triggers inflammation responses in chronic obstructive sleep apnea rat model.PloS one · 2026Article
- GRPR-induced FAM135A expression promote perineural invasion in prostate cancer.Molecular cancer · 2025Article
- Inhibition of PGK1 ameliorates acute kidney injury through inactivating the PKM2/ALOX12/ferroptosis pathway in a study with male mice.Nature communications · 2025Article
- PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025Article
- Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Design, Synthesis, and Evaluation of New 2-Arylpropanoic Acid-l-Tryptophan Derivatives for Mitigating Cisplatin-Induced Nephrotoxicity.Molecules (Basel, Switzerland) · 2025Article
- IGF-Binding Protein 7 and Cadmium-Induced Hepatorenal Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
- Establishment of an anaplastic stratification signature for gastric cancer based on diverse regulated cell-death.Frontiers in immunology · 2025Article
- Evaluation of a tumor marker gastrin-releasing peptide precursor in the patients with kidney injuries.American journal of cancer research · 2025Article
- Loss of LRP1 Promotes Hepatocellular Carcinoma Progression via UFL1-Mediated Activation of NF-κB Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Gastrin-releasing peptide receptor antagonist RC-3095 inhibits Porphyromonas gingivalis lipopolysaccharide-accelerated atherosclerosis by suppressing inflammatory responses in endothelial cells and macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Regulated necrosis role in inflammation and repair in acute kidney injury.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 5 institutions in 3 countries.
Chao LiInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Qiu-Ying MaDepartment of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Anhui Public Health Clinical Center, No. 100 Huaihai Road, Hefei 230012, China.
Xue-Qi LiuDepartment of Nephrology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Hai-di LiInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Ming-Jun YuSchool of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China.
Shuai-Shuai XieInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Wen-Xian MaInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Ying ChenInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Jia-Nan WangInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Ruo-Bing HeInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
He-Ge BianDepartment of Pharmacology, School of Basic Medical Sciences, Key Laboratory of Anti-inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei 230032, China.
Yuan HeInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Li GaoDepartment of Nephrology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Sheng-Song DengSchool of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China.
Hong-Mei ZangInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Qian GongDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China.
Jia-Gen WenInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Ming-Ming LiuInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Chen YangInstitute of Nephrology, Affiliated Hospital of Guangdong Medical University, 57 Renmin Road, Zhanjiang 524001, China.
Hai-Yong ChenDepartment of Chinese Medicine, The University of Hong Kong-Shenzhen Hospital, The University of Hong Kong, Shenzhen 518009, China.
Jun LiInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Hui-Yao LanDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, and Liu Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong, Shatin, Hong Kong 999077, China.
Juan JinDepartment of Pharmacology, School of Basic Medical Sciences, Key Laboratory of Anti-inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei 230032, China. Electronic address: jinjuan@ahmu.edu.cn.
Ri-Sheng YaoSchool of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China. Electronic address: rishengyao@163.com.
Xiao-Ming MengInflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China. Electronic address: mengxiaoming@ahmu.edu.cn.
Anhui Medical University · CNHefei University of Technology · CNChinese University of Hong Kong · HKGuangdong Medical College · CNUniversity of Hong Kong - Shenzhen Hospital · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrin-releasing peptide (GRP) binds to its receptor (GRP receptor [GRPR]) to regulate multiple biological processes, but the function of GRP/GRPR axis in acute kidney injury (AKI) remains unknown. In the present study, GRPR is highly expressed by tubular epithelial cells (TECs) in patients or mice with AKI, while histone deacetylase 8 may lead to the transcriptional activation of GRPR. Functionally, we uncovered that GRPR was pathogenic in AKI, as genetic deletion of GRPR was able to protect mice from cisplatin- and ischemia-induced AKI. This was further confirmed by specifically deleting the GRPR gene from TECs in GRPR
Indexed as
Acute Kidney InjuryCisplatinAnimalsInflammationKidneyMiceMice, Inbred C57BLNecroptosisCisplatinacute kidney injuryGRPGRPRinflammationnecroptosisSTAT1
Identifiers
What Socratic holds
Textmetadata
Read underepoch 390
Registered trials
None linked
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 Socratic graph.