Evidence map›Paper›PMID 30466736›Full record

ArticleThe American journal of the medical sciences2019

Advanced Glycation End Products Stimulate Angiotensinogen Production in Renal Proximal Tubular Cells.

Joseph M Garagliano, Akemi Katsurada, Kayoko Miyata, Andrei V Derbenev, Andrea Zsombok, L Gabriel Navar, Ryousuke Satou

Open access · greenAbstract read
In one paragraph

Article in The American journal of the medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  6. Article
  7. The Triad NaInternational journal of molecular sciences · 2023
    Article
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  10. Observational
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  12. Review
  13. Review
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  15. Article
  16. Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020
    Review
  17. Article
  18. 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

7 authors at 1 institution in 1 country.

Joseph M GaraglianoDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Akemi KatsuradaDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Kayoko MiyataDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Andrei V DerbenevDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Andrea ZsombokDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
L Gabriel NavarDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Ryousuke SatouDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana. Electronic address: rsato@tulane.edu.
Tulane University · US

Funding

Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
Histone deacetylase 9 is an epigenetic suppressor of intrarenal angiotensinogen, serving as a key mechanism in angiotensinogen augmentation in hypertensionR01DK107694 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI SATO, RYOSUKE · 2016 to 2020
$1.4M
NIDDK NIH HHS R01 DK107694NIGMS NIH HHS P30 GM103337
6 · The paper itself

Abstract

backgroundElevated advanced glycation end products (AGE) in diabetes mellitus (DM) are implicated in the progression of DM-associated tissue injury, including diabetic nephropathy. The intrarenal renin-angiotensin system, in particular augmentation of angiotensinogen (AGT) in proximal tubular cells (PTC), plays a crucial role in the development of diabetic nephropathy. This study investigated hypothesis that AGE stimulates AGT production in PTC. MATERIALS AND

methodsUrinary AGT and AGE levels in streptozotocin-induced DM mice were measured by enzyme-linked immunosorbent assays. AGT expression and secretion were evaluated in cultured rat PTC receiving 0-200 µg/ml AGE-BSA treatments for 24 hours. Furthermore, intracellular signaling pathways activated by AGE were elucidated.

resultsDM mice exhibited greater urinary AGT and AGE levels compared to control mice (AGT: 21.6 ± 5.5 ng/day vs. 190.1 ± 57.8 ng/day, AGE: 139.1 ± 21.6 μg/day vs. 332.8 ± 102.7 μg/day). In cultured PTC, treatment with AGE-BSA enhanced AGT mRNA expression (3.43 ± 0.11-fold compared to control), intracellular AGT protein levels (3.60 ± 0.38-fold), and secreted AGT levels (2.11 ± 0.18-fold). On the other hand, AGT levels were not altered in PTC receiving nonglycated BSA. Recombinant soluble AGE receptor, which competes with endogenous AGE receptor, diminished the AGE-induced AGT upregulation, suggesting that AGE-BSA stimulates AGT expression via activation of the AGE receptor. Enhanced phosphorylation of ERK1/2 and c-Jun, but not p38 MAP kinase, were observed in AGE-BSA-treated PTC. AGE-induced AGT augmentation was attenuated by an ERK inhibitor.

conclusionsThe findings indicate that AGE enhances proximal tubular AGT expression via ERK1/2, which can exacerbate the development of diabetic related kidney injury.

Indexed as

AngiotensinogenAnimalsCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesGlycation End Products, AdvancedKidney Tubules, ProximalMaleMiceMice, Inbred C57BLRenin-Angiotensin SystemSignal TransductionAgt protein, mouseAngiotensinogenGlycation End Products, AdvancedAdvanced glycation end productsAngiotensinogenDiabetes mellitusKidneyRenal proximal tubules

Identifiers

PMID30466736
PMCPMC6778966
OpenAlexW2898520759

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.