Evidence map›Paper›PMID 21511693›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Chronic nicotine exposure exacerbates acute renal ischemic injury.

Istvan Arany, Samira Grifoni, Jeb S Clark, Eva Csongradi, Christine Maric, Luis A Juncos

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Atmospheric stressors and kidney diseases.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Cigarette Smoking and Risk of Hospitalization With Acute Kidney Injury: The Atherosclerosis Risk in Communities (ARIC) Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024
    Observational
  20. 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

6 authors at 2 institutions in 3 countries.

Istvan AranyDept. of Pediatrics, Div. of Pediatric Nephrology, University of Mississippi Medical Center, Research Wing Rm. R127, 2500 N. State St., Jackson, MS 39216, USA. iarany@umc.edu
Samira Grifoni
Jeb S Clark
Eva Csongradi
Christine Maric
Luis A Juncos
Institute of Molecular Biology and Biophysics · RUUniversity of Debrecen · HU

Funding

Supressor ANGII Determines Acute & Chronic Renal InjuryR01DK073401 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI JUNCOS, LUIS A. · 2006 to 2010
$1.6M
NIDDK NIH HHS DK073401
6 · The paper itself

Abstract

Recent epidemiological reports showed that smoking has a negative impact on renal function and elevates the renal risk not only in the renal patient but perhaps also in the healthy population. Studies suggested that nicotine, a major tobacco alkaloid, links smoking to renal dysfunction. While several studies showed that smoking/chronic nicotine exposure exacerbates the progression of chronic renal diseases, its impact on acute kidney injury is virtually unknown. Here, we studied the effects of chronic nicotine exposure on acute renal ischemic injury. We found that chronic nicotine exposure increased the extent of renal injury induced by warm ischemia-reperfusion as evidenced by morphological changes, increase in plasma creatinine level, and kidney injury molecule-1 expression. We also found that chronic nicotine exposure elevated markers of oxidative stress such as nitrotyrosine as well as malondialdehyde. Interestingly, chronic nicotine exposure alone increased oxidative stress and injury in the kidney without morphological alterations. Chronic nicotine treatment not only increased reactive oxygen species (ROS) production and injury but also exacerbated oxidative stress-induced ROS generation through NADPH oxidase and mitochondria in cultured renal proximal tubule cells. The resultant oxidative stress provoked injury through JNK-mediated activation of the activator protein (AP)-1 transcription factor in vitro. This mechanism might exist in vivo as phosphorylation of JNK and its downstream target c-jun, a component of the AP-1 transcription factor, is elevated in the ischemic kidneys exposed to chronic nicotine. Our results imply that smoking may sensitize the kidney to ischemic insults and perhaps facilitates progression of acute kidney injury to chronic kidney injury.

Indexed as

Acute Kidney InjuryAdenoviridaeAnimalsBlotting, WesternCell LineCells, CulturedCell SurvivalCotinineIschemiaKidneyKidney Tubules, ProximalLuciferasesMaleMalondialdehydeMAP Kinase Kinase 4MiceCotinineLuciferasesMalondialdehydeMAP Kinase Kinase 4NicotineNicotinic AgonistsReactive Oxygen SpeciesTranscription Factor AP-1

Identifiers

PMID21511693
PMCPMC3129886
OpenAlexW2053442494

What OpenQuestion holds

Textmetadata
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.