Evidence map›Paper›PMID 26739891›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy.

Wenzhen Xiao, Ying Fan, Niansong Wang, Peter Y Chuang, Kyung Lee, John Cijiang He

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. 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
2.5field-weighted citation impact, top 13% 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, 32 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Wenzhen XiaoDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and Department of Nephrology, Shanghai Six Municipal Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China cijiang.he@mssm.edu.
Ying FanDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and Department of Nephrology, Shanghai Six Municipal Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Niansong WangDepartment of Nephrology, Shanghai Six Municipal Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Peter Y ChuangDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and.
Kyung LeeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and.
John Cijiang HeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and.
Icahn School of Medicine at Mount Sinai · USShanghai Sixth People's Hospital · CN

Funding

VIRAL PATHOGENESIS OF HIV ASSOCIATED NEPHROPATHYP01DK056492 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HE, JOHN CIJIANG · 1999 to 2021
$27.8M
Role of HIPK2 in Kidney Tubulointerstitial InjuryR01DK088541 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2010 to 2019
$4.0M
Cellular and molecular mechanisms of retinoids in podocytesR01DK078897 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2007 to 2018
$3.6M
Role of RTN1A in the Progression of Diabetic NephropathyR01DK109683 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2016 to 2023
$3.3M
SIRT1 Sirtuin in Diabetic Kidney DiseaseR01DK098126 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHUANG, PETER YENLUNG · 2014 to 2018
$1.7M
NIDDK NIH HHS 1-R01-DK-078897NIDDK NIH HHS 1-R01-DK-088541NIDDK NIH HHS 1-R01-DK-098126-01A1NIDDK NIH HHS P01-DK-56492NIDDK NIH HHS R01 DK088541NIDDK NIH HHS R01 DK109683
6 · The paper itself

Abstract

Our previous studies have suggested a critical role of reticulon (RTN)1A in mediating endoplasmic reticulum (ER) stress in kidney cells of animal models and humans with kidney diseases. A large body of evidence suggests that proteinuria itself can cause tubular cell injury leading to the progression of kidney disease. In the present study, we determined whether RTN1A mediates proteinuria-induced tubular cell injury through increased ER stress. We found that incubation of HK2 cells with human serum albumin induced the expression of RTN1A and ER stress markers, whereas knockdown of RTN1A expression attenuated human serum albumin-induced ER stress and tubular cell apoptosis in vitro. In vivo, we found that tubular cell-specific RTN1 knockdown resulted in a significant attenuation of tubular cell ER stress, apoptosis, and renal fibrosis in a model of albumin overload nephropathy. Based on these findings, we conclude that RTN1A is a key mediator for proteinuria-induced tubular cell toxicity and renal fibrosis.

Indexed as

Serum Albumin, BovineAlbuminuriaAnimalsApoptosisDisease Models, AnimalDisease ProgressionEndoplasmic Reticulum StressFibrosisGenotypeHEK293 CellsHumansKidney TubulesMice, KnockoutNerve Tissue ProteinsPhenotypeRenal Insufficiency, ChronicALB protein, humanNerve Tissue ProteinsRTN1 protein, humanRtn1 protein, mouseSerum AlbuminSerum Albumin, BovineSerum Albumin, Humanapoptosisendoplasmic reticulum stresskidney diseaseproteinuriarenal tubular cellsreticulon-1

Identifiers

PMID26739891
PMCPMC4773829
OpenAlexW2226839947

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.