Evidence map›Paper›PMID 28271468›Full record

ReviewCurrent diabetes reports2017

The Role of Endoplasmic Reticulum Stress in Diabetic Nephropathy.

Ying Fan, Kyung Lee, Niansong Wang, John Cijiang He

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.8field-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

66 citing papers in PubMed, 108 citations in OpenAlex.

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  6. Zingerone alleviates diabetic nephropathy by interrupting the ER stress-inflammation-apoptosis cascade in streptozotocin-induced diabetic mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
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6 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Ying FanDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Kyung LeeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L Levy Place, Box 1243, New York, NY, 10029, USA.
Niansong WangDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
John Cijiang HeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L Levy Place, Box 1243, New York, NY, 10029, USA. cijiang.he@mssm.edu.
Icahn School of Medicine at Mount Sinai · USShanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CN

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
NIDDK NIH HHS P30 DK079307
6 · The paper itself

Abstract

purpose of reviewDiabetic nephropathy (DN) has become the leading cause of end-stage renal disease (ESRD) worldwide. Accumulating evidence suggests that endoplasmic reticulum (ER) stress plays a major role in the development and progression of DN. Recent findings suggested that many attributes of DN, such as hyperglycemia, proteinuria, and increased advanced glycation end products and free fatty acids, can all trigger unfolded protein response (UPR) in kidney cells. Herein, we review the current knowledge on the role of ER stress in the setting of kidney injury with a specific emphasis on DN. RECENT

findingsAs maladaptive ER stress response caused by excessively prolonged UPR will eventually cause cell death and increase kidney injury, several ER stress inhibitors have been shown to improve DN in animal models, albeit blocking both adaptive and maladaptive UPR. More recently, reticulon-1A (RTN1A), an ER-associated protein, was shown to be increased in both human and mouse diabetic kidneys. Its expression correlates with the progression of DN, and its polymorphisms are associated with kidney disease in people with diabetes. Increased RTN1A expression heightened the ER stress response and renal cell apoptosis, and conversely reduced RTN1A in renal cells decreased apoptosis and ameliorated kidney injury and DN progression, suggesting that RTN1A may be a novel target to specifically restrain the maladaptive UPR. These findings suggest that ER stress response in renal cells is a key driver of progression of DN and that the inhibition of the unchecked ER stress response in DN, such as by inhibition of RTN1A function, may be a promising therapeutic approach against DN.

Indexed as

AnimalsDiabetic NephropathiesEndoplasmic Reticulum StressHumansKidney TubulesMesangial CellsNerve Tissue ProteinsUnfolded Protein ResponseNerve Tissue ProteinsRTN1 protein, humanApoptosisDiabetic nephropathyEndoplasmic reticulum stressReticulon-1 (RTN-1)Unfolded protein response

Identifiers

PMID28271468
OpenAlexW2593083600

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.