Evidence map›Paper›PMID 22749805›Full record

ArticleFree radical biology & medicine2012

Poor lysosomal membrane integrity in proximal tubule cells of haptoglobin 2-2 genotype mice with diabetes mellitus.

Rabea Asleh, Farid M Nakhoul, Rachel Miller-Lotan, Hoda Awad, Dan Farbstein, Nina S Levy, Nakhoul Nakhoul, Theodore C Iancu, Irena Manov, Michael Laue and 3 more

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Deoxynivalenol Exposure Leads to Abnormal Renal Tubular Autophagy Flow.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Lysosomal dysfunction-induced autophagic stress in diabetic kidney disease.Journal of cellular and molecular medicine · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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

13 authors at 5 institutions in 3 countries.

Rabea AslehDepartment of Anatomy and Cell Biology, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, 1 Efron St. Bat Galim, POB 9649, Haifa, Israel. asl@yahoo.com
Farid M Nakhoul
Rachel Miller-Lotan
Hoda Awad
Dan Farbstein
Nina S Levy
Nakhoul Nakhoul
Theodore C Iancu
Irena Manov
Michael Laue
Maret G Traber
Katie M Lebold
Andrew P Levy
Technion – Israel Institute of Technology · ILOregon State University · USBar-Ilan University · ILPoriya Medical Center · ILRobert Koch Institute · DE

Funding

The Oxidation Hypothesis Revisited:Haptoglobin Genotype and Diabetic AtheroscleroR01DK085226 · NIDDK · TECHNION-ISRAEL INSTITUTE OF TECHNOLOGY · PI LEVY, ANDREW PETER · 2009 to 2013
$664k
NIDDK NIH HHS R01 DK085226NIDDK NIH HHS R01DK085226
6 · The paper itself

Abstract

The haptoglobin (Hp) genotype is a major determinant of progression of nephropathy in individuals with diabetes mellitus (DM). The major function of the Hp protein is to bind and modulate the fate of extracorpuscular hemoglobin and its iron cargo. We have previously demonstrated an interaction between the Hp genotype and the DM on the accumulation of iron in renal proximal tubule cells. The primary objective of this study was to determine the intracellular localization of this iron in the proximal tubule cell and to assess its potential toxicity. Transmission electron microscopy demonstrated a marked accumulation of electron-dense deposits in the lysosomes of proximal tubules cells in Hp 2-2 DM mice. Energy-dispersive X-ray spectroscopy and electron energy loss spectroscopy were used to perform elemental analysis of these deposits and demonstrated that these deposits were iron rich. These deposits were associated with lysosomal membrane lipid peroxidation and loss of lysosomal membrane integrity. Vitamin E administration to Hp 2-2 DM mice resulted in a significant decrease in both intralysosomal iron-induced oxidation and lysosomal destabilization. Iron-induced renal tubular injury may play a major role in the development of diabetic nephropathy and may be a target for slowing the progression of renal disease.

Indexed as

AnimalsAntioxidantsbeta-N-AcetylhexosaminidasesDiabetes Mellitus, ExperimentalDiabetic NephropathiesGenotypeHaptoglobinsIntracellular MembranesIronKidney Tubules, ProximalLipid PeroxidationLysosomesMiceMice, Inbred C57BLOxidation-ReductionOxidative StressAntioxidantsbeta-N-AcetylhexosaminidasesHaptoglobinsIronVitamin E

Identifiers

PMID22749805
PMCPMC3600120
OpenAlexW1992798213

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.