Evidence map›Paper›PMID 25349246›Full record

ReviewThe Journal of endocrinology2015

Autophagy in diabetic nephropathy.

Yan Ding, Mary E Choi

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 2 pooled it
13.7field-weighted citation impact, top 1% 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

164 citing papers in PubMed, 2 syntheses or guidelines pooled it, 304 citations in OpenAlex.

  1. Pooled it
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  12. Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.International journal of molecular sciences · 2025
    Review
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104 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

2 authors at 1 institution in 1 country.

Yan DingDivision of Nephrology and HypertensionJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, 525 East 68th Street, Box 3, New York, New York 10065, USA.
Mary E ChoiDivision of Nephrology and HypertensionJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, 525 East 68th Street, Box 3, New York, New York 10065, USA mechoi@med.cornell.edu.
Cornell University · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
TGF-beta signaling in the kidneyR01DK057661 · NIDDK · YALE UNIVERSITY · PI CHOI, MARY E · 2000 to 2014
$4.1M
Heme oxygenase-1: Regulation and Function in CaveolaeR01HL079904 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2005 to 2014
$2.9M
NHLBI NIH HHS P01 HL114501NHLBI NIH HHS P01-HL114501NHLBI NIH HHS R01 HL079904NHLBI NIH HHS R01-HL079904NIDDK NIH HHS R01 DK057661NIDDK NIH HHS R01-DK57661
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the most common cause of end-stage kidney disease worldwide, and is associated with increased morbidity and mortality in patients with both type 1 and type 2 diabetes. Increasing prevalence of diabetes has made the need for effective treatment of DN critical and thereby identifying new therapeutic targets to improve clinical management. Autophagy is a highly conserved 'self-eating' pathway by which cells degrade and recycle macromolecules and organelles. Autophagy serves as an essential mechanism to maintain homeostasis of glomeruli and tubules, and plays important roles in human health and diseases. Impairment of autophagy is implicated in the pathogenesis of DN. Emerging body of evidence suggests that targeting the autophagic pathway to activate and restore autophagy activity may be renoprotective. In this review, we examine current advances in our understanding of the roles of autophagy in diabetic kidney injury, focusing on studies in renal cells in culture, human kidney tissues, and experimental animal models of diabetes. We discuss the major nutrient-sensing signal pathways and diabetes-induced altered intracellular metabolism and cellular events, including accumulation of advanced glycation end-products, increased oxidative stress, endoplasmic reticulum stress, hypoxia, and activation of the renin-angiotensin system, which modulate autophagic activity and contribute to the development of DN. We also highlight recent studies of autophagy and transforming growth factor-β in renal fibrosis, the final common response to injury that ultimately leads to end-stage kidney failure in both type 1 and type 2 diabetes. These findings suggest the possibility that autophagy can be a therapeutic target against DN.

Indexed as

AnimalsAutophagyDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic NephropathiesHumansKidneySignal TransductionTOR Serine-Threonine KinasesTOR Serine-Threonine Kinasesautophagydiabetes mellituskidneymacroautophagynephropathy

Identifiers

PMID25349246
PMCPMC4238413
OpenAlexW2104785025

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.