Evidence map›Paper›PMID 24284520›Full record

ArticleKidney international2014

Podocyte injury enhances filtration of liver-derived angiotensinogen and renal angiotensin II generation.

Taiji Matsusaka, Fumio Niimura, Ira Pastan, Ayumi Shintani, Akira Nishiyama, Iekuni Ichikawa

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Taiji Matsusaka1] Department of Internal Medicine, Tokai University School of Medicine, Isehara, Japan [2] Institute of Medical Science, Tokai University School of Medicine, Isehara, Japan.
Fumio NiimuraDepartment of Pediatrics, Tokai University School of Medicine, Isehara, Japan.
Ira PastanLaboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Ayumi Shintani1] Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee, USA [2] Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Akira NishiyamaDepartment of Pharmacology, Research Equipment Center, and Second Department of Internal Medicine, Kagawa University School of Medicine, Kagawa, Japan.
Iekuni Ichikawa1] Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA [2] Tokai University School of Medicine, Isehara, Japan [3] Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Tokai University · JPKagawa University · JPNational Cancer Institute · USVanderbilt University Medical Center · US

Funding

Immunotoxin Therapy of Solid and Hematopoietic Tumors: Preclinical StudiesZIABC008753 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PASTAN, IRA · 2009 to 2024
$33.1M
Growth Regulation SectionZ01BC010298 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PASTAN, IRA · 1998 to 2008
$2.1M
Intramural NIH HHS Z01 BC010298
6 · The paper itself

Abstract

Intrarenal angiotensin II is increased in kidney diseases independently of plasma angiotensin II and is thought to promote progressive deterioration of renal architecture. Here we investigated the mechanism of enhanced renal angiotensin II generation in kidney glomerular diseases. For this, kidney- or liver-specific angiotensinogen gene (Agt) knockout was superimposed on the mouse model of inducible podocyte injury (NEP25). Seven days after induction of podocyte injury, renal angiotensin II was increased ninefold in NEP25 mice with intact Agt, accompanied by increases in urinary albumin and angiotensinogen excretion, renal angiotensinogen protein, and its mRNA. Kidney Agt knockout attenuated renal Agt mRNA but not renal angiotensin II, renal, or urinary angiotensinogen protein. In contrast, liver Agt knockout markedly reduced renal angiotensin II to 18.7% of that of control NEP25 mice, renal and urinary angiotensinogen protein, but not renal Agt mRNA. Renal angiotensin II had no relationship with renal Agt mRNA, or with renal renin mRNA, which was elevated in liver Agt knockouts. Kidney and liver dual Agt knockout mice showed phenotypes comparable to those of liver Agt knockout mice. Thus, increased renal angiotensin II generation upon severe podocyte injury is attributed to increased filtered angiotensinogen of liver origin resulting from loss of macromolecular barrier function of the glomerular capillary wall that occurs upon severe podocyte injury.

Indexed as

AlbuminuriaAngiotensin IIAngiotensinogenAnimalsAntibodies, MonoclonalDisease Models, AnimalExotoxinsGenotypeKidney DiseasesKidney Tubules, ProximalLiverMembrane ProteinsMice, KnockoutPhenotypePodocytesRNA, MessengerAgt protein, mouseAngiotensin IIAngiotensinogenAntibodies, MonoclonalB3(Fv)-PE38KDEL recombinant immunotoxinExotoxinsMembrane ProteinsnephrinRNA, MessengerSodium

Identifiers

PMID24284520
PMCPMC7681568
OpenAlexW2075836698

What Socratic 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 Socratic graph.