Evidence map›Paper›PMID 29187372›Full record

ArticleAmerican journal of physiology. Renal physiology2018

Renal tubular ACE-mediated tubular injury is the major contributor to microalbuminuria in early diabetic nephropathy.

Masahiro Eriguchi, Mercury Lin, Michifumi Yamashita, Tuantuan V Zhao, Zakir Khan, Ellen A Bernstein, Susan B Gurley, Romer A Gonzalez-Villalobos, Kenneth E Bernstein, Jorge F Giani

Open access · bronzeAbstract readComparative Study
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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023
    Article
  6. Knockout of ACE-N facilitates improved cardiac function after myocardial infarction.Journal of molecular and cellular cardiology plus · 2023
    Article
  7. Article
  8. Protective effect ofChinese herbal medicines · 2023
    Article
  9. Article
  10. Article
  11. Novel roles of the renal angiotensin-converting enzyme.Molecular and cellular endocrinology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  19. Review
  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

10 authors at 2 institutions in 1 country.

Masahiro EriguchiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Mercury LinDepartments of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center , Los Angeles, California.
Michifumi YamashitaDepartments of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center , Los Angeles, California.
Tuantuan V ZhaoDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Zakir KhanDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Ellen A BernsteinDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Susan B GurleyDivision of Nephrology, Department of Medicine, Duke University School of Medicine , Durham, North Carolina.
Romer A Gonzalez-VillalobosDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Kenneth E BernsteinDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.
Jorge F GianiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles, California.ORCID 0000-0003-0481-6595
Cedars-Sinai Medical Center · USDuke University · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2016 to 2020
$12.4M
Actions of Angiotensin II Along the Nephron to Regulate Blood PressureR01DK098382 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GURLEY, SUSAN BAILEY · 2014 to 2025
$3.8M
RAS and InjuryR01HL110353 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2011 to 2015
$2.2M
Renal ACE, salt sensitivity and blood pressure controlR03DK101592 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI GONZALEZ-VILLALOBOS, ROMER ANDRES · 2014 to 2016
$638k
Carboxypeptidase ACE and MHC Class I PresentationR21AI114965 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2015 to 2016
$481k
NCATS NIH HHS UL1 TR001881NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL110353NIAID NIH HHS R21 AI114965NIDDK NIH HHS R01 DK098382NIDDK NIH HHS R03 DK101592
6 · The paper itself

Abstract

Diabetic nephropathy is a major cause of end-stage renal disease in developed countries. While angiotensin-converting enzyme (ACE) inhibitors are used to treat diabetic nephropathy, how intrarenal ACE contributes to diabetic renal injury is uncertain. Here, two mouse models with different patterns of renal ACE expression were studied to determine the specific contribution of tubular vs. glomerular ACE to early diabetic nephropathy: it-ACE mice, which make endothelial ACE but lack ACE expression by renal tubular epithelium, and ACE 3/9 mice, which lack endothelial ACE and only express renal ACE in tubular epithelial cells. The absence of endothelial ACE normalized the glomerular filtration rate and endothelial injury in diabetic ACE 3/9 mice. However, these mice developed tubular injury and albuminuria and displayed low renal levels of megalin that were similar to those observed in diabetic wild-type mice. In diabetic it-ACE mice, despite hyperfiltration, the absence of renal tubular ACE greatly reduced tubulointerstitial injury and albuminuria and increased renal megalin expression compared with diabetic wild-type and diabetic ACE 3/9 mice. These findings demonstrate that endothelial ACE is a central regulator of the glomerular filtration rate while tubular ACE is a key player in the development of tubular injury and albuminuria. These data suggest that tubular injury, rather than hyperfiltration, is the main cause of microalbuminuria in early diabetic nephropathy.

Indexed as

AlbuminuriaAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEndothelial CellsGlomerular Filtration RateKidney GlomerulusKidney TubulesLow Density Lipoprotein Receptor-Related Protein-2Mice, KnockoutPeptidyl-Dipeptidase ARNA, Small InterferingStreptozocinLow Density Lipoprotein Receptor-Related Protein-2Lrp2 protein, mousePeptidyl-Dipeptidase ARNA, Small InterferingStreptozocinangiotensin-converting enzymeglomerular hyperfiltrationmegalinmicroalbuminuriatubulointerstitial fibrosis

Identifiers

PMID29187372
PMCPMC5966765
OpenAlexW2769518750

What OpenQuestion 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 OpenQuestion graph.