Evidence map›Paper›PMID 20466987›Full record

ReviewCirculation research2010

Aldose reductase and cardiovascular diseases, creating human-like diabetic complications in an experimental model.

Ravichandran Ramasamy, Ira J Goldberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.2field-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

61 citing papers in PubMed, 161 citations in OpenAlex.

  1. Trial
  2. Review
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  6. Article
  7. Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Ferroptosis-A Shared Mechanism for Parkinson's Disease and Type 2 Diabetes.International journal of molecular sciences · 2024
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Ravichandran RamasamyDepartment of Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA. rr260@columbia.edu
Ira J Goldberg
Columbia College · CA

Funding

VASCULAR AND MONOCYTE DYSFUNCTION IN WOUND REPAIRP01HL060901 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI YAN, SHI FANG · 1999 to 2017
$20.2M
Regulation and function of plasma lipid transfer proteinsP01HL054591 · NHLBI · ROCKEFELLER UNIVERSITY · PI TALL, ALAN RICHARD · 1995 to 2010
$19.9M
TRANSGENIC MOUSE AND ANIMAL MANAGEMENTP01AG026467 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHMIDT, ANN MARIE · 2008 to 2014
$9.2M
Creating Glucose Responsive Cardiovascular Complications U01HL087945 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA J · 2006 to 2010
$2.0M
ALDOSE REDUCTASE AND CARDIAC ISCHEMIC INJURYR01HL061783 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI RAMASAMY, RAVICHANDRAN · 1999 to 2006
$1.9M
POLYOL PATHWAY AND ISCHEMIC INJURY IN DIABETIC HEARTSR01HL068954 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI RAMASAMY, RAVICHANDRAN · 2002 to 2005
$981k
Hyperglycemia, Aldose Reducatse &Murine AtherosclerosisR01DK072147 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA JAY · 2005 to 2005
$306k
NHLBI NIH HHS P01 HL054591NHLBI NIH HHS P01 HL060901NHLBI NIH HHS P01-HL54591NHLBI NIH HHS P01-HL6091NHLBI NIH HHS R01 HL061783NHLBI NIH HHS R01 HL068954NHLBI NIH HHS R01-HL61783NHLBI NIH HHS R01-HL68954NHLBI NIH HHS U01 HL087945NHLBI NIH HHS U01-HL0879450NIA NIH HHS P01 AG026467NIDDK NIH HHS R01 DK072147
6 · The paper itself

Abstract

Hyperglycemia and reduced insulin actions affect many biological processes. One theory is that aberrant metabolism of glucose via several pathways including the polyol pathway causes cellular toxicity. Aldose reductase (AR) is a multifunctional enzyme that reduces aldehydes. Under diabetic conditions AR converts glucose into sorbitol, which is then converted to fructose. This article reviews the biology and pathobiology of AR actions. AR expression varies considerably among species. In humans and rats, the higher level of AR expression is associated with toxicity. Flux via AR is increased by ischemia and its inhibition during ischemia reperfusion reduces injury. However, similar pharmacological effects are not observed in mice unless they express a human AR transgene. This is because mice have much lower levels of AR expression, probably insufficient to generate toxic byproducts. Human AR expression in LDL receptor knockout mice exacerbates vascular disease, but only under diabetic conditions. In contrast, a recent report suggests that genetic ablation of AR increased atherosclerosis and increased hydroxynonenal in arteries. It was hypothesized that AR knockout prevented reduction of toxic aldehydes. Like many in vivo effects found in genetically manipulated animals, interpretation requires the reproduction of human-like physiology. For AR, this will require tissue specific expression of AR in sites and at levels that approximate those in humans.

Indexed as

Disease Models, AnimalAldehyde ReductaseAnimalsCardiovascular DiseasesDiabetes ComplicationsDiabetes Mellitus, ExperimentalHumansAldehyde Reductase

Identifiers

PMID20466987
PMCPMC2882633
OpenAlexW2016654742

What Socratic 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 Socratic graph.