Evidence map›Paper›PMID 9399945›Full record

ArticleThe Journal of clinical investigation1997

Immunohistochemical colocalization of glycoxidation products and lipid peroxidation products in diabetic renal glomerular lesions. Implication for glycoxidative stress in the pathogenesis of diabetic nephropathy.

K Horie, T Miyata, K Maeda, S Miyata, S Sugiyama, H Sakai, C van Ypersole de Strihou, V M Monnier, J L Witztum, K Kurokawa

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In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
16.6field-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

90 citing papers in PubMed, 431 citations in OpenAlex.

  1. Trial
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  4. High levels of oxidized LDL in circulating immune complexes are associated with increased odds of developing abnormal albuminuria in Type 1 diabetes.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2012
    Trial
  5. Article
  6. Article
  7. Serum Levels of NBiomedicines · 2025
    Article
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  9. Review
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  11. Article
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  15. Molecules (Basel, Switzerland) · 2022
    Article
  16. Review
  17. Article
  18. Reversal of hypertriglyceridemia in diabetic BTBR ob/ob mice does not prevent nephropathy.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  19. Article
  20. Review

30 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

10 authors at 7 institutions in 3 countries.

K HorieDepartment of Internal Medicine, Nagoya University School of Medicine, Nagoya 461, Japan.
T Miyata
K Maeda
S Miyata
S Sugiyama
H Sakai
C van Ypersole de Strihou
V M Monnier
J L Witztum
K Kurokawa
Tokai University · JPCase Western Reserve University · USChukyo Hospital · JPKobe University · JPNagoya University · JPUCLouvain · BEUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end products (AGEs) include a variety of protein adducts whose accumulation alters the structure and function of tissue proteins and stimulates cellular responses. They have been implicated in tissue damage associated with diabetic complications. To assess the possible link between AGE accumulation and the development of diabetic nephropathy (DN), we have examined the immunohistochemical localization of various AGE structures postulated to date, i.e., pentosidine, Nepsilon-(carboxymethyl)lysine (CML), and pyrraline, in diabetic and control kidneys. CML and pentosidine accumulate in the expanded mesangial matrix and thickened glomerular capillary walls of early DN and in nodular lesions and arterial walls of advanced DN, but were absent in control kidneys. By contrast, pyrraline was not found within diabetic glomeruli but was detected in the interstitial connective tissue of both normal and diabetic kidneys. Although the distribution of pyrraline was topographically identical to type III collagen, distribution of pentosidine and CML was not specific for collagen type, suggesting that difference in matrix protein composition per se could not explain heterogeneous AGE localization. Since oxidation is linked closely to the formation of pentosidine and CML, we also immunostained malondialdehyde (MDA), a lipid peroxidation product whose formation is accelerated by oxidative stress, assuming that local oxidative stress may serve as a mechanism of pentosidine and CML accumulation. Consistent with our assumption, diabetic nodular lesions were stained positive for MDA. These findings show that AGE localization in DN varies according to AGE structure, and suggest that the colocalization of markers of glycoxidation (pentosidine and CML) with a marker of lipid peroxidation reflects a local oxidative stress in association with the pathogenesis of diabetic glomerular lesions. Thus, glycoxidation markers may serve as useful biomarkers of oxidative damage in DN.

Indexed as

AdolescentAdultAgedAnimalsAntibodiesArginineCollagenDiabetes Mellitus, Type 2Diabetic NephropathiesFemaleGlycation End Products, AdvancedHumansImmunoenzyme TechniquesKidney GlomerulusLipid PeroxidationLysine2-formyl-5-(hydroxymethyl)pyrrole-1-norleucineAntibodiesArginineCollagenGlycation End Products, AdvancedLysineMalondialdehydeN(6)-carboxymethyllysineNorleucinepentosidinePyrroles

Identifiers

PMID9399945
PMCPMC508511
OpenAlexW2085341182

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.