Evidence map›Paper›PMID 23062986›Full record

ReviewSeminars in nephrology2012

Can we target tubular damage to prevent renal function decline in diabetes?

Joseph V Bonventre

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Observational
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  6. Article
  7. Article
  8. SGLT2 inhibitors and acute kidney injury.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  9. Research progress on the regulation of miRNAs in diabetic kidney disease and osteoporosis.International journal of clinical and experimental pathology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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50 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

1 author at 1 institution in 1 country.

Joseph V BonventreRenal Division, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, MA, USA. joseph_bonventre@hms.harvard.edu
Harvard University · US

Funding

KIDNEY INJURY MOLECULE-1 IN EPITHELIAL REPAIRR01DK072381 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2025
$8.6M
Mechanisms of Ischemic Kidney Injury and RepairR01DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI JOSEPH VINCENT BONVENTRE · 1987 to 2026
$6.2M
Mechanisms of Ischemic Kidney Injury and RepairR37DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1993 to 2021
$5.2M
TWO NOVEL CPLA2 BINDING PROTEINS AND CELL DEATHR01DK054741 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1999 to 2010
$2.5M
Two novel cPLA2 binding proteins and cell deathR56DK054741 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI SHERIDAN, ALICE MARIE · 2005 to 2005
$168k
NIDDK NIH HHS DK054741NIDDK NIH HHS DK39773NIDDK NIH HHS DK72381NIDDK NIH HHS R01 DK039773NIDDK NIH HHS R01 DK054741NIDDK NIH HHS R01 DK072381NIDDK NIH HHS R37 DK039773NIDDK NIH HHS R56 DK054741
6 · The paper itself

Abstract

The glomerulus has been at the center of attention as the primary site of injury in diabetic nephropathy (DN). Although there is no question that there are changes seen in the glomerulus, it is also well known that tubulointerstitial changes are a prominent component of the disease, especially in patients with type 2 diabetes. The level of albuminuria and DN disease progression best correlate with tubular degeneration and interstitial fibrosis. Nephrotoxicity studies in animals reveal that albuminuria is a highly sensitive marker of early tubular toxicity even in the absence of glomerular pathology. Urinary biomarker data in human beings support the view that proximal tubule injury contributes in a primary way, rather than in a secondary manner, to the development of early DN. I present a model in which very specific injury to the proximal tubule in vivo in the mouse results in severe inflammation, loss of blood vessels, interstitial fibrosis, and glomerulosclerosis. Increased glucose levels, free glycation adducts, reactive oxygen species, and oxidized lipids result in toxicity to tubule epithelia. This results in loss of cells with a stimulus to repair the epithelium. However, because of sublethal injury there is cell-cycle arrest in epithelial cells attempting to replace damaged cells. This leads to epithelial secretion of both profibrogenic growth factors, collagens, and factors that cause pericytes to proliferate and differentiate into myofibroblasts, leading to endothelial destabilization and capillary rarefaction. Local ischemia ensues with further injury to the tubules, more profibrogenic mediators, matrix protein deposition, fibrosis, and glomerulosclerosis.

Indexed as

AnimalsDiabetic NephropathiesDisease Models, AnimalDisease ProgressionFibrosisHepatitis A Virus Cellular Receptor 1HumansKidney GlomerulusKidney TubulesMembrane GlycoproteinsMiceReceptors, VirusHAVCR1 protein, humanHepatitis A Virus Cellular Receptor 1Membrane GlycoproteinsReceptors, Virus

Identifiers

PMID23062986
PMCPMC3595316
OpenAlexW2074580711

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.