Evidence map›Paper›PMID 25207878›Full record

ArticleKidney international2015

Renal denervation prevents long-term sequelae of ischemic renal injury.

Jinu Kim, Babu J Padanilam

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Neuroimmune Control of Inflammation in Acute Kidney Injury and Multiorgan Dysfunction.Journal of the American Society of Nephrology : JASN · 2025
    Review
  10. Article
  11. The organum vasculosum of the lamina terminalis contributes to neurohumoral mechanisms of renal vascular hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Neuroimmune interplay in kidney health and disease: Role of renal nerves.Autonomic neuroscience : basic & clinical · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Jinu Kim1] Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, USA [2] Department of Anatomy, Jeju National University School of Medicine, Jeju, Republic of Korea.
Babu J Padanilam1] Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, USA [2] Department of Internal Medicine, Section of Nephrology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
University of Nebraska Medical Center · US

Funding

Regulation of Apoptosis in Renal IschemiaR01DK083291 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2010 to 2013
$1.3M
Mechanisms of selective glycolytic inhibition in ischemic kidney proximal tublesR56DK090332 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2012 to 2012
$150k
NIDDK NIH HHS DK-083291NIDDK NIH HHS DK-090332NIDDK NIH HHS R01 DK083291NIDDK NIH HHS R56 DK090332
6 · The paper itself

Abstract

Signals that drive interstitial fibrogenesis after renal ischemia reperfusion injury remain undefined. Sympathetic activation manifests even in the early clinical stages of chronic kidney disease and is directly related to disease severity. A role for renal nerves in renal interstitial fibrogenesis in the setting of ischemia reperfusion injury has not been studied. In male 129S1/SvImJ mice, ischemia reperfusion injury induced tubulointerstitial fibrosis as indicated by collagen deposition and profibrotic protein expression 4 to 16 days after the injury. Leukocyte influx, proinflammatory protein expression, oxidative stress, apoptosis, and cell cycle arrest at G2/M phase were enhanced after ischemia reperfusion injury. Renal denervation at the time of injury or up to 1 day post injury improved histology, decreased proinflammatory/profibrotic responses and apoptosis, and prevented G2/M cell cycle arrest in the kidney. Treatment with afferent nerve-derived calcitonin gene-related peptide (CGRP) or efferent nerve-derived norepinephrine in denervated and ischemia reperfusion injury-induced kidneys mimicked innervation, restored inflammation and fibrosis, induced G2/M arrest, and enhanced TGF-β1 activation. Blocking norepinephrine or CGRP function using respective receptor blockers prevented these effects. Consistent with the in vivo study, treatment with either norepinephrine or CGRP induced G2/M cell cycle arrest in HK-2 proximal tubule cells, whereas antagonists against their respective receptors prevented G2/M arrest. Thus, renal nerve stimulation is a primary mechanism and renal nerve-derived factors drive epithelial cell cycle arrest and the inflammatory cascade causing interstitial fibrogenesis after ischemia reperfusion injury.

Indexed as

DenervationAcute Kidney InjuryAnimalsCalcitonin Gene-Related PeptideDisease Models, AnimalFibrosisG2 Phase Cell Cycle CheckpointsKidneyMaleMiceMice, 129 StrainNorepinephrineOxidative StressRenal Insufficiency, ChronicReperfusion InjurySignal TransductionCalcitonin Gene-Related PeptideNorepinephrineTransforming Growth Factor beta1

Identifiers

PMID25207878
PMCPMC4312521
OpenAlexW2035115018

What OpenQuestion holds

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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.