Evidence map›Paper›PMID 33711514›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2021

Identification of novel therapeutic targets for contrast induced acute kidney injury (CI-AKI): alpha blockers as a therapeutic strategy for CI-AKI.

Sreenivasulu Kilari, Amit Sharma, Chenglei Zhao, Avishek Singh, Chuanqi Cai, Michael Simeon, Andre J van Wijnen, Sanjay Misra

Open access · greenAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Sreenivasulu KilariVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Amit SharmaVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Chenglei ZhaoVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Vascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Avishek SinghVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Chuanqi CaiVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Michael SimeonVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Andre J van WijnenDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota; Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota.
Sanjay MisraVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota; Department of Pulmonary and Critical Care Medicine Mayo Clinic, Rochester, Minnesota. Electronic address: misra.sanjay@mayo.edu.
Mayo Clinic · US

Funding

The Role of Hypoxia In Venous Neointimal Hyperplasia In Hemodialysis GraftsR01HL098967 · NHLBI · MAYO CLINIC ROCHESTER · PI Sanjay Misra · 2010 to 2026
$10.4M
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR01DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2017 to 2019
$716k
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR56DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2020 to 2020
$103k
NHLBI NIH HHS R01 HL098967NIDDK NIH HHS R01 DK107870NIDDK NIH HHS R56 DK107870
6 · The paper itself

Abstract

Iodinated contrast is used for imaging and invasive procedures and it can cause contrast induced acute kidney injury (CI-AKI), which is the third leading hospital-acquired health problem. The purpose of the present study was to determine the effect of α-adrenergic receptor-1b (Adra1b) inhibition by using terazosin on change in kidney function, gene, and protein expression in C57BL/6J male mice, 6-8 weeks with chronic kidney disease (CKD). CKD was induced by surgical nephrectomy. Twenty eight days later, 100-µL of iodinated contrast (CI group) or saline (S group) was given via the carotid artery. Whole-transcriptome RNA-sequencing (RNA-Seq) analysis of the kidneys was performed at day 2. Mice received either 50-µL of saline ip or terazosin (2 mg/kg) in 50-µL of saline ip 1 hour before contrast administration which was continued every 12 hours until the animals were euthanized 2 and 7 days later. The kidneys were removed for gene expression, immunohistochemical analysis, and blood serum analyzed for kidney function. Differential gene expression analysis identified 21 upregulated and 436 downregulated genes (fold change >2; P < 0.05) that were common to all sample (n = 3 for both contrast and saline). We identified Adra1b using bioinformatic analysis. Mice treated with terazosin had a significant decrease in serum creatinine, urinary Kim-1 levels, HIF-1α, apoptosis, and downstream Adrab1 genes including Ece1, Edn1, pMAPK14 with increased cell proliferation. Contrast exposure upregulated Adra1b gene expression in HK-2 cells. Inhibition of Adra1b with terazosin abrogated Ece1, Edn1, and contrast-induced Fsp-1, Mmp-2, Mmp-9 expression, and caspase-3/7 activity in HK-2 cells.

Indexed as

Acute Kidney InjuryAdrenergic alpha-1 Receptor AntagonistsAnimalsApoptosisCell ProliferationCells, CulturedContrast MediaEndothelin-Converting EnzymesMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 14PrazosinReceptors, Adrenergic, alpha-1Adrenergic alpha-1 Receptor AntagonistsContrast MediaEce1 protein, mouseEndothelin-Converting EnzymesMitogen-Activated Protein Kinase 14PrazosinReceptors, Adrenergic, alpha-1Terazosin

Identifiers

PMID33711514
PMCPMC8328880
OpenAlexW3134169065

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.