Evidence map›Paper›PMID 31537053›Full record

ReviewKidney research and clinical practice2019

Mechanisms and therapeutic targets of ischemic acute kidney injury.

Sang Jun Han, H Thomas Lee

Open access · diamondAbstract readReview
In one paragraph

Review in Kidney research and clinical practice, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
17.1field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 253 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Rewiring the mitochondrial NADMaterials today. Bio · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

89 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

2 authors at 1 institution in 1 country.

Sang Jun HanDepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA.ORCID http://orcid.org/0000-0002-5425-9056
H Thomas LeeDepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA.ORCID http://orcid.org/0000-0002-4367-7594
Columbia University · US

Funding

Paneth cells and acute kidney injuryR01DK109544 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, H. THOMAS · 2017 to 2021
$1.8M
Peptidylarginine deiminase-4 and acute kidney injuryR01DK115694 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, H. THOMAS · 2017 to 2021
$1.6M
NIDDK NIH HHS R01 DK109544NIDDK NIH HHS R01 DK115694
6 · The paper itself

Abstract

Acute kidney injury (AKI) due to renal ischemia reperfusion (IR) is a major clinical problem without effective therapy and is a significant and frequent cause of morbidity and mortality during the perioperative period. Although the pathophysiology of ischemic AKI is not completely understood, several important mechanisms of renal IR-induced AKI have been studied. Renal ischemia and subsequent reperfusion injury initiates signaling cascades mediating renal cell necrosis, apoptosis, and inflammation, leading to AKI. Better understanding of the molecular and cellular pathophysiological mechanisms underlying ischemic AKI will provide more targeted approach to prevent and treat renal IR injury. In this review, we summarize important mechanisms of ischemic AKI, including renal cell death pathways and the contribution of endothelial cells, epithelial cells, and leukocytes to the inflammatory response during ischemic AKI. Additionally, we provide some updated potential therapeutic targets for the prevention or treatment of ischemic AKI, including Toll-like receptors, adenosine receptors, and peptidylarginine deiminase 4. Finally, we propose mechanisms of ischemic AKI-induced liver, intestine, and kidney dysfunction and systemic inflammation mainly mediated by Paneth cell degranulation as a potential explanation for the high mortality observed with AKI.

Indexed as

Acute kidney injuryApoptosisInflammationIschemia reperfusion injuryMechanismNecrosis

Identifiers

PMID31537053
PMCPMC6913588
OpenAlexW2974257765

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.