Evidence map›Paper›PMID 31373312›Full record

ArticleInternational journal of molecular sciences2019

Kidney Injury Molecule-1 Is Upregulated in Renal Lipotoxicity and Mediates Palmitate-Induced Tubular Cell Injury and Inflammatory Response.

Xueying Zhao, Xiaoming Chen, Yuanyuan Zhang, Jasmine George, Alyssa Cobbs, Guoshen Wang, Lingyun Li, Nerimiah Emmett

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Metabolites · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. 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 1 country.

Xueying ZhaoDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA. xzhao@msm.edu.ORCID 0000-0003-0857-2823
Xiaoming ChenDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Yuanyuan ZhangDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Jasmine GeorgeDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.ORCID 0000-0002-6999-5099
Alyssa CobbsDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Guoshen WangDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.ORCID 0000-0002-8420-6465
Lingyun LiDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Nerimiah EmmettDepartment of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Morehouse School of Medicine · US

Funding

Kidney injury molecule-1 in diabetic nephropathySC1DK112151 · NIDDK · MOREHOUSE SCHOOL OF MEDICINE · PI ZHAO, XUEYING · 2016 to 2019
$1.4M
NIDDK NIH HHS SC1 DK112151NIH HHS 8U54MD007588NIH HHS SC1DK112151
6 · The paper itself

Abstract

Diabetic nephropathy is increasingly recognized as a major contributor to kidney failure in patients with obesity and type 2 diabetes. This study was designed to identify the molecular mediators of kidney injury associated with metabolic syndrome with or without hyperglycemia. We compared renal gene expression profiles in Zucker lean (ZL), Zucker obese (ZO), and Zucker diabetic (ZD) rats using cDNA microarray with quantitative verification of selected transcripts by real-time PCR. Compared to the 20-week-old ZL control (glucose: 110 ± 8 mg/dL), both prediabetic ZO (glucose: 157 ± 11 mg/dL) and diabetic ZD (glucose: 481 ± 37 mg/dL) rats displayed hyperlipidemia and kidney injury with a high degree of proteinuria. cDNA microarray identified 25 inflammation and injury-related transcriptomes whose expression levels were similarly increased in ZO and ZD kidneys. Among them, kidney injury molecule-1 (KIM-1) was found to be the most highly upregulated in both ZO and ZD kidneys. Immunofluorescence staining of kidney sections revealed a strong correlation between lipid overload and KIM-1 upregulation in proximal tubules of ZO and ZD rats. In cultured primary renal tubular epithelial cells (TECs), administration of saturated fatty acid palmitate resulted in an upregulation of KIM-1, osteopontin, and CD44, which was greatly attenuated by U0126, an inhibitor of extracellular signal-regulated kinase (ERK)1/2. Moreover, knockdown of KIM-1 by siRNA interference inhibited palmitate-induced cleaved caspase-3, osteopontin, and CD44 proteins in primary TECs. Our results indicate that KIM-1 expression is upregulated in renal lipotoxicity and may play an important role in fatty acid-induced inflammation and tubular cell damage in obesity and diabetic kidney disease.

Indexed as

AnimalsCaspase 3Cell Adhesion MoleculesDiabetic NephropathiesGene Expression ProfilingHyaluronan ReceptorsHyperglycemiaHyperlipidemiasKidney TubulesMetabolic SyndromeObesityOsteopontinPalmitatesProteinuriaRatsRats, ZuckerCaspase 3Cell Adhesion MoleculesHavcr1 protein, ratHyaluronan ReceptorsOsteopontinPalmitatesRNA, Small Interferinginflammationlipotoxicitymetabolic syndromenephropathy

Identifiers

PMID31373312
PMCPMC6679556
OpenAlexW2958997923

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.