Evidence map›Paper›PMID 40121405›Full record

ReviewBMC nephrology2025

Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.

Jiajia He, Yanqin Chen, Yi Li, Yunlin Feng

Abstract readReview
In one paragraph

Review in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. 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

4 authors.

Jiajia HeDepartment of Nephrology, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yanqin ChenDepartment of Nephrology, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yi LiDepartment of Nephrology and Institute of Nephrology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Sichuan Clinical Research Centre for Kidney Diseases, Chengdu, 610072, China.
Yunlin FengDepartment of Nephrology and Institute of Nephrology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Sichuan Clinical Research Centre for Kidney Diseases, Chengdu, 610072, China. fengyunlin@med.uestc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is a clinical challenge characterized by elevated morbidity and a substantial impact on individual health and socioeconomic factors. A comprehensive examination of the molecular pathways behind AKI is essential for its prevention and management. In recent years, vigorous research in the domain of AKI has concentrated on pathophysiological characteristics, early identification, and therapeutic approaches across many aetiologies and highlighted the principal themes of oxidative stress, inflammatory response, apoptosis, necrosis, and immunological response. This review comprehensively reviewed the molecular mechanisms underlying AKI, including oxidative stress, inflammatory pathways, immune cell-mediated injury, activation of the renin-angiotensin-aldosterone (RAAS) system, mitochondrial damage and autophagy, apoptosis, necrosis, etc. Inflammatory pathways are involved in the injuries in all four structural components of the kidney. We also summarized therapeutic techniques and pharmacological agents associated with the aforementioned molecular pathways. This work aims to clarify the molecular mechanisms of AKI thoroughly, offer novel insights for further investigations of AKI, and facilitate the formulation of efficient therapeutic methods to avert the progression of AKI.

Indexed as

Acute Kidney InjuryAnimalsApoptosisAutophagyHumansInflammationOxidative StressRenin-Angiotensin SystemAcute kidney injuryComplementInflammationMolecular mechanismsOxidative stressTherapeutic interventions

Identifiers

PMID40121405
PMCPMC11929251

What OpenQuestion holds

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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.