Evidence map›Paper›PMID 28931523›Full record

ArticleAmerican journal of physiology. Renal physiology2018

Contribution of myo-inositol oxygenase in AGE:RAGE-mediated renal tubulointerstitial injury in the context of diabetic nephropathy.

Isha Sharma, Rashmi S Tupe, Aryana K Wallner, Yashpal S Kanwar

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  10. Review
  11. Article
  12. Review
  13. Regulated cell death in cisplatin-induced AKI: relevance ofAmerican journal of physiology. Renal physiology · 2021
    Article
  14. Article
  15. Article
  16. The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  17. Diabetes · 2020
    Article
  18. Inositols and metabolic disorders: From farm to bedside.Journal of traditional and complementary medicine · 2020
    Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Isha SharmaDepartments of Pathology and Medicine, Northwestern University , Chicago, Illinois.
Rashmi S TupeBiochemical Sciences Division, Rajiv Gandhi Institute of IT and Biotechnology, Bharati Vidyapeeth University , Pune , India.
Aryana K WallnerDepartments of Pathology and Medicine, Northwestern University , Chicago, Illinois.
Yashpal S KanwarDepartments of Pathology and Medicine, Northwestern University , Chicago, Illinois.
Northwestern University · USBharati Vidyapeeth Deemed University · IN

Funding

Pathogenesis of Diabetic NephropathyR01DK060635 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2002 to 2023
$6.6M
NIDDK NIH HHS R01 DK060635
6 · The paper itself

Abstract

Advanced glycation end products (AGEs) play a role in pathogenesis of diabetic nephropathy (DN). Myo-inositol oxygenase (MIOX) has been implicated in tubulointerstitial injury in the context of DN. We investigated the effect of AGEs on MIOX expression and delineated mechanisms that lead to tubulointerstitial injury. The status of MIOX, RAGE, and relevant cellular signaling pathways activated following AGE:RAGE interaction was examined in tubular cells and kidneys of AGE-BSA-treated mice. A solid-phase assay revealed an enhanced binding of RAGE with AGE-BSA, AGE-laminin, and AGE-collagen IV. The cells treated with AGE-BSA had increased MIOX activity/expression and promoter activity. This was associated with activation of various signaling kinases of phosphatidylinositol 3-kinase (PI3K)-AKT pathway and increased expression of NF-κB, transforming growth factor (TGF)-β, and fibronectin, which was negated with the treatment of MIOX/RAGE- small interfering (si) RNA. Concomitant with MIOX upregulation, there was an increased generation of reactive oxygen species (ROS), which could be abrogated with MIOX/RAGE- siRNA treatment. The kidneys of mice treated with AGE-BSA had significantly high urinary A/C ratio, upregulation of MIOX, RAGE and NF-κB, along with influx of monocytes into the tubulointerstitium, increased the expression of MCP-1, IL-6, and fibronectin and increased the generation of ROS. Such perturbations were abrogated with the concomitant treatment of inhibitors MIOX or RAGE (d-glucarate and FPS-ZM1). These studies support a role of AGE:RAGE interaction in the activation of PI3K-AKT pathway and upregulation of MIOX, with excessive generation of ROS, increased expression of NF-κB, inflammatory cytokines, TGF-β, and fibronectin. Collectively, these observations highlight the relevance of the biology of MIOX in the contribution toward tubulointerstitial injury in DN.

Indexed as

Diabetic NephropathiesFibronectinsGlycation End Products, AdvancedInositol OxygenaseKidneyPhosphatidylinositol 3-KinasesReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsSerum Albumin, Bovineadvanced glycation end products-bovine serum albuminFibronectinsGlycation End Products, AdvancedInositol OxygenasePhosphatidylinositol 3-KinasesReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsSerum Albumin, Bovinediabetesglycationmyo-inositol oxygenasereactive oxygen species

Identifiers

PMID28931523
PMCPMC5866356
OpenAlexW2753937739

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.