Evidence map›Paper›PMID 26916346›Full record

ArticleScientific reports2016

Autophagy is activated to protect against endotoxic acute kidney injury.

Shuqin Mei, Man Livingston, Jielu Hao, Lin Li, Changlin Mei, Zheng Dong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

4 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

6 authors at 3 institutions in 2 countries.

Shuqin MeiKidney Institute, Department of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Man LivingstonDepartment of Cellular Biology and Anatomy, Medical College of Georgia, Georgia Regents University and Charlie Norwood VA Medical Center, Augusta, Georgia.
Jielu HaoKidney Institute, Department of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Lin LiKidney Institute, Department of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Changlin MeiKidney Institute, Department of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zheng DongDepartment of Cellular Biology and Anatomy, Medical College of Georgia, Georgia Regents University and Charlie Norwood VA Medical Center, Augusta, Georgia.
Second Military Medical University · CNAugusta University · USCentral South University · CN

Funding

DNA methylation in kidney repair after ischemic AKIR01DK058831 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI DONG, ZHENG · 2001 to 2025
$7.5M
Kidney Injury by Cisplatin and Renoprotective Strategies.R01DK087843 · NIDDK · AUGUSTA UNIVERSITY · PI DONG, ZHENG · 2010 to 2025
$5.8M
Molecular Regulation of Ischemic Renal FailureI01BX000319 · VA · CHARLIE NORWOOD VA MEDICAL CENTER · PI Zheng Dong · 2009 to 2026
–
BLRD VA I01 BX000319NIDDK NIH HHS R01 DK058831NIDDK NIH HHS R01 DK087843
6 · The paper itself

Abstract

Endotoxemia in sepsis, characterized by systemic inflammation, is a major cause of acute kidney injury (AKI) in hospitalized patients, especially in intensive care unit; however the underlying pathogenesis is poorly understood. Autophagy is a conserved, cellular catabolic pathway that plays crucial roles in cellular homeostasis including the maintenance of cellular function and viability. The regulation and role of autophagy in septic or endotoxic AKI remains unclear. Here we show that autophagy was induced in kidney tubular cells in mice by the endotoxin lipopolysaccharide (LPS). Pharmacological inhibition of autophagy with chloroquine enhanced LPS-induced AKI. Moreover, specific ablation of autophagy gene 7 (Atg7) from kidney proximal tubules worsened LPS-induced AKI. Together, the results demonstrate convincing evidence of autophagy activation in endotoxic kidney injury and support a renoprotective role of autophagy in kidney tubules.

Indexed as

Acute Kidney InjuryAnimalsAutophagyAutophagy-Related Protein 7ChloroquineCisplatinEndotoxemiaKidney Tubules, ProximalLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutReperfusion InjuryAtg7 protein, mouseAutophagy-Related Protein 7ChloroquineCisplatinLipopolysaccharides

Identifiers

PMID26916346
PMCPMC4768171
OpenAlexW2284572479

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Registered trials

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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.