Evidence map›Paper›PMID 24353183›Full record

ArticleDiabetes2014

Rap1 ameliorates renal tubular injury in diabetic nephropathy.

Li Xiao, Xuejing Zhu, Shikun Yang, Fuyou Liu, Zhiguang Zhou, Ming Zhan, Ping Xie, Dongshan Zhang, Jun Li, Panai Song and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

76 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
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  10. The Noncanonical Wnt5a-CaJournal of cellular and molecular medicine · 2025
    Article
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  14. Review
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  18. Article
  19. Article
  20. Role of renal tubular programed cell death in diabetic kidney disease.Diabetes/metabolism research and reviews · 2023
    Review

16 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

12 authors at 3 institutions in 2 countries.

Li XiaoDepartment of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuejing Zhu
Shikun Yang
Fuyou Liu
Zhiguang Zhou
Ming Zhan
Ping Xie
Dongshan Zhang
Jun Li
Panai Song
Yashpal S Kanwar
Lin Sun
Second Xiangya Hospital of Central South University · CNCentral South University · CNNorthwestern University · US

Funding

Pathogenesis of Diabetic NephropathyR01DK060635 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2002 to 2023
$6.6M
NIDDK NIH HHS R01 DK060635
6 · The paper itself

Abstract

Rap1b ameliorates high glucose (HG)-induced mitochondrial dysfunction in tubular cells. However, its role and precise mechanism in diabetic nephropathy (DN) in vivo remain unclear. We hypothesize that Rap1 plays a protective role in tubular damage of DN by modulating primarily the mitochondria-derived oxidative stress. The role and precise mechanisms of Rap1b on mitochondrial dysfunction and of tubular cells in DN were examined in rats with streptozotocin (STZ)-induced diabetes that have Rap1b gene transfer using an ultrasound microbubble-mediated technique as well as in renal proximal epithelial tubular cell line (HK-2) exposed to HG ambiance. The results showed that Rap1b expression decreased significantly in tubules of renal biopsies from patients with DN. Overexpression of a constitutively active Rap1b G12V notably ameliorated renal tubular mitochondrial dysfunction, oxidative stress, and apoptosis in the kidneys of STZ-induced rats, which was accompanied with increased expression of transcription factor C/EBP-β and PGC-1α. Furthermore, Rap1b G12V also decreased phosphorylation of Drp-1, a key mitochondrial fission protein, while boosting the expression of genes related to mitochondrial biogenesis and antioxidants in HK-2 cells induced by HG. These effects were imitated by transfection with C/EBP-β or PGC-1α short interfering RNA. In addition, Rap1b could modulate C/EBP-β binding to the endogenous PGC-1α promoter and the interaction between PGC-1α and catalase or mitochondrial superoxide dismutase, indicating that Rap1b ameliorates tubular injury and slows the progression of DN by modulation of mitochondrial dysfunction via C/EBP-β-PGC-1α signaling.

Indexed as

AnimalsAntioxidantsApoptosisCCAAT-Enhancer-Binding Protein-betaCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesHumansKidneyKidney TubulesMaleMitochondriaOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpharap GTP-Binding ProteinsRatsAntioxidantsCCAAT-Enhancer-Binding Protein-betaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratRAP1B protein, humanRap1b protein, ratrap GTP-Binding ProteinsTranscription Factors

Identifiers

PMID24353183
PMCPMC3964498
OpenAlexW2138393223

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.