Evidence map›Paper›PMID 30101366›Full record

ArticleArchives of pharmacal research2018

D-ribose induces nephropathy through RAGE-dependent NF-κB inflammation.

Jinni Hong, Xuemei Wang, Ning Zhang, Hong Fu, Weiwei Li

Open access · hybridAbstract read
In one paragraph

Article in Archives of pharmacal research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Mechanistic Study ofDrug design, development and therapy · 2023
    Article
  12. Review
  13. Article
  14. Protein Modification with Ribose GeneratesInternational journal of molecular sciences · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

5 authors at 2 institutions in 2 countries.

Jinni HongIntegrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China.
Xuemei WangIntegrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China.
Ning ZhangIntegrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China.
Hong FuIntegrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China.
Weiwei LiIntegrated Laboratory of Traditional Chinese Medicine and Western Medicine, Peking University First Hospital, Beijing, 100034, People's Republic of China. weiwei_ivy@163.com.ORCID http://orcid.org/0000-0002-2048-0780
Peking University · CNVirginia Commonwealth University · US

Funding

National Natural Science Foundation of China 81530099National Natural Science Foundation of China 81573763Natural Science Foundation of Beijing Municipality 7172221State's Key Project of Research and Development Plan 2016YFE0116200
6 · The paper itself

Abstract

Recently, aberrantly high levels of D-ribose have been discovered in type II diabetic patients. D-ribose glycates proteins more rapidly than D-glucose, resulting in the production of advanced glycation end products (AGEs). Accumulations of these products can be found in impaired renal function, but the mechanisms are poorly understood. The present study tested whether D-ribose induces renal dysfunction via the RAGE-dependent NF-κB signaling pathway. In vivo, administration of D-ribose was found to lower blood glucose and regulate insulin tolerance. Compared to controls, urine nitrogen and creatinine excretion were increased in mice receiving D-ribose and were accompanied by severe pathological renal damage. Furthermore, immunohistochemistry showed that NF-κB, AGEs, and receptor of AGEs (RAGE) increased in the kidneys of the mice with D-ribose treatment. In vitro, by western blot and immunofluorescent staining, we confirmed that D-ribose induced NF-κB activation and accumulation of AGEs and RAGE in mesangial cells. By co-immunoprecipitation, we found that the pull-down of RAGE remarkably increased the expression of NF-κB. Silencing the RAGE gene blocked the phosphorylation of NF-κB induced by D-ribose. These results strongly suggest that D-ribose induced NF-κB inflammation in a RAGE-dependent manner, which may be a triggering mechanism leading to nephropathy.

Indexed as

AnimalsBlood GlucoseCells, CulturedDiabetic NephropathiesDown-RegulationInflammationInjections, IntraperitonealKidneyMaleMiceMice, Inbred BALB CNF-kappa BPhosphorylationReceptor for Advanced Glycation End ProductsRiboseBlood GlucoseNF-kappa BReceptor for Advanced Glycation End ProductsRiboseAGEsDiabetesKidneyRAGE

Identifiers

PMID30101366
PMCPMC6132794
OpenAlexW2885209821

What OpenQuestion holds

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Registered trials

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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.