Evidence map›Paper›PMID 31226747›Full record

ReviewInternational journal of molecular sciences2019

Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury.

Sara J Holditch, Carolyn N Brown, Andrew M Lombardi, Khoa N Nguyen, Charles L Edelstein

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

195 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Rewiring the mitochondrial NADMaterials today. Bio · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026
    Article
  11. Molecules (Basel, Switzerland) · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026
    Review
  19. Article
  20. Article

135 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

5 authors.

Sara J HolditchDivision of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA. sara.holditch@ucdenver.edu.
Carolyn N BrownDivision of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA. CAROLYN.N.BROWN@UCDENVER.EDU.
Andrew M LombardiDivision of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA. anlo5057@colorado.edu.
Khoa N NguyenDivision of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA. KHOA.N.NGUYEN@UCDENVER.EDU.
Charles L EdelsteinDivision of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA. Charles.edelstein@ucdenver.edu.

Funding

PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1M
BLRD VA I01 BX003803NIGMS NIH HHS T32 GM007635U.S. Department of Defense W81XWH-16-1-0172.U.S. Department of Veterans Affairs BX003803-01A1
6 · The paper itself

Abstract

Cisplatin is a widely used chemotherapeutic agent used to treat solid tumours, such as ovarian, head and neck, and testicular germ cell. A known complication of cisplatin administration is acute kidney injury (AKI). The development of effective tumour interventions with reduced nephrotoxicity relies heavily on understanding the molecular pathophysiology of cisplatin-induced AKI. Rodent models have provided mechanistic insight into the pathophysiology of cisplatin-induced AKI. In the subsequent review, we provide a detailed discussion of recent advances in the cisplatin-induced AKI phenotype, principal mechanistic findings of injury and therapy, and pre-clinical use of AKI rodent models. Cisplatin-induced AKI murine models faithfully develop gross manifestations of clinical AKI such as decreased kidney function, increased expression of tubular injury biomarkers, and tubular injury evident by histology. Pathways involved in AKI include apoptosis, necrosis, inflammation, and increased oxidative stress, ultimately providing a translational platform for testing the therapeutic efficacy of potential interventions. This review provides a discussion of the foundation laid by cisplatin-induced AKI rodent models for our current understanding of AKI molecular pathophysiology.

Indexed as

Acute Kidney InjuryAnimalsAntineoplastic AgentsCisplatinDisease Models, AnimalHumansKidneyNeoplasmsAntineoplastic AgentsCisplatinacute kidney injuryAKIapoptosiscisplatininflammationoxidative stress

Identifiers

PMID31226747
PMCPMC6627318

What Socratic holds

Textmetadata
LicenceCC BY
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.